# gene_set_details

systematic_name: M8147
exact_source: GSE22611_3477_200_UP
source_species_code: HS
GEO_id: GSE22611
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in HEK293 cells over-expressing wildtype NOD2 [GeneID=64127]: untreated versus muramyl dipeptide [PubChem=11620162] for 6h.

description_full:
  NOD2 is an intracellular receptor for the bacterial cell wall component muramyl dipeptide (MDP) and variants of NOD2 are associated with chronic inflammatory diseases of barrier organs e.g. Crohn disease, asthma and atopic eczema. It is known that activation of NOD2 induces a variety of inflammatory and antibacterial factors. The exact transcriptomal signatures that define the cellular programs downstream of NOD2 activation and the influence of the Crohn-associated variant L1007fsinsC are yet to be defined. To describe the MDP-induced activation program, we analyzed the transcriptomal reactions of isogenic HEK293 cells expressing NOD2wt or NOD2L1007fsinsC to stimulation with MDP. Importantly, a clear loss-of-function could be observed in the cells carrying the Crohn-associated variant L1007fsinsC, while the NOD2wt cells showed differential regulation of growth factors, chemokines and several antagonists of NF-κB, e.g. TNFAIP3 (A20) and IER3.


systematic_name: M8148
exact_source: GSE22611_3480_200_DN
source_species_code: HS
GEO_id: GSE22611
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in HEK293 cells at 6h after stimulation by muramyl dipeptide [PubChem=11620162]: over-expressing mutant NOD2 [GeneID=64127] versus control.

description_full:
  NOD2 is an intracellular receptor for the bacterial cell wall component muramyl dipeptide (MDP) and variants of NOD2 are associated with chronic inflammatory diseases of barrier organs e.g. Crohn disease, asthma and atopic eczema. It is known that activation of NOD2 induces a variety of inflammatory and antibacterial factors. The exact transcriptomal signatures that define the cellular programs downstream of NOD2 activation and the influence of the Crohn-associated variant L1007fsinsC are yet to be defined. To describe the MDP-induced activation program, we analyzed the transcriptomal reactions of isogenic HEK293 cells expressing NOD2wt or NOD2L1007fsinsC to stimulation with MDP. Importantly, a clear loss-of-function could be observed in the cells carrying the Crohn-associated variant L1007fsinsC, while the NOD2wt cells showed differential regulation of growth factors, chemokines and several antagonists of NF-κB, e.g. TNFAIP3 (A20) and IER3.


systematic_name: M8151
exact_source: GSE22611_3475_200_UP
source_species_code: HS
GEO_id: GSE22611
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in HEK293 cells over-expressing wildtype NOD2 [GeneID=64127]: untreated versus muramyl dipeptide [PubChem=11620162] for 2h.

description_full:
  NOD2 is an intracellular receptor for the bacterial cell wall component muramyl dipeptide (MDP) and variants of NOD2 are associated with chronic inflammatory diseases of barrier organs e.g. Crohn disease, asthma and atopic eczema. It is known that activation of NOD2 induces a variety of inflammatory and antibacterial factors. The exact transcriptomal signatures that define the cellular programs downstream of NOD2 activation and the influence of the Crohn-associated variant L1007fsinsC are yet to be defined. To describe the MDP-induced activation program, we analyzed the transcriptomal reactions of isogenic HEK293 cells expressing NOD2wt or NOD2L1007fsinsC to stimulation with MDP. Importantly, a clear loss-of-function could be observed in the cells carrying the Crohn-associated variant L1007fsinsC, while the NOD2wt cells showed differential regulation of growth factors, chemokines and several antagonists of NF-κB, e.g. TNFAIP3 (A20) and IER3.


systematic_name: M8152
exact_source: GSE22611_3475_200_DN
source_species_code: HS
GEO_id: GSE22611
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in HEK293 cells over-expressing wildtype NOD2 [GeneID=64127]: untreated versus muramyl dipeptide [PubChem=11620162] for 2h.

description_full:
[cell repeats an earlier one in this file: 955 characters]


systematic_name: M8157
exact_source: GSE22611_3480_200_UP
source_species_code: HS
GEO_id: GSE22611
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in HEK293 cells at 6h after stimulation by muramyl dipeptide [PubChem=11620162]: over-expressing mutant NOD2 [GeneID=64127] versus control.

description_full:
[cell repeats an earlier one in this file: 955 characters]


systematic_name: M8158
exact_source: GSE22611_3476_200_UP
source_species_code: HS
GEO_id: GSE22611
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in HEK293 cells expressing mutant NOD2 [GeneID=64127]: untreated versus muramyl dipeptide [PubChem=11620162] for 2h.

description_full:
[cell repeats an earlier one in this file: 955 characters]


systematic_name: M8159
exact_source: GSE22611_3839_200_UP
source_species_code: HS
GEO_id: GSE22611
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in HEK293 cells at 6h after stimulation by muramyl dipeptide [PubChem=11620162]: over-expressing wildtype NOD2 [GeneID=64127] versus control.

description_full:
[cell repeats an earlier one in this file: 955 characters]


systematic_name: M8160
exact_source: GSE22611_3839_200_DN
source_species_code: HS
GEO_id: GSE22611
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in HEK293 cells at 6h after stimulation by muramyl dipeptide [PubChem=11620162]: over-expressing wildtype NOD2 [GeneID=64127] versus control.

description_full:
[cell repeats an earlier one in this file: 955 characters]


systematic_name: M8161
exact_source: GSE22611_3840_200_UP
source_species_code: HS
GEO_id: GSE22611
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in HEK293 cells at 2h after stimulation by muramyl dipeptide [PubChem=11620162]: over-expressing mutant NOD2 [GeneID=64127] versus control.

description_full:
[cell repeats an earlier one in this file: 955 characters]


systematic_name: M8162
exact_source: GSE22611_3478_200_UP
source_species_code: HS
GEO_id: GSE22611
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in HEK293 cells expressing mutant NOD2 [GeneID=64127]: untreated versus muramyl dipeptide [PubChem=11620162] for 6h.

description_full:
[cell repeats an earlier one in this file: 955 characters]


systematic_name: M8163
exact_source: GSE22611_3478_200_DN
source_species_code: HS
GEO_id: GSE22611
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in HEK293 cells expressing mutant NOD2 [GeneID=64127]: untreated versus muramyl dipeptide [PubChem=11620162] for 6h.

description_full:
[cell repeats an earlier one in this file: 955 characters]


systematic_name: M8164
exact_source: GSE22611_3472_200_UP
source_species_code: HS
GEO_id: GSE22611
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in HEK293 cells expressing: wildtype NOD2 [GeneID=64127] versus mutant NOD2 [GeneID=64127].

description_full:
[cell repeats an earlier one in this file: 955 characters]


systematic_name: M8165
exact_source: GSE22611_3472_200_DN
source_species_code: HS
GEO_id: GSE22611
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in HEK293 cells expressing: wildtype NOD2 [GeneID=64127] versus mutant NOD2 [GeneID=64127].

description_full:
[cell repeats an earlier one in this file: 955 characters]


systematic_name: M8173
exact_source: GSE22611_3477_200_DN
source_species_code: HS
GEO_id: GSE22611
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in HEK293 cells over-expressing wildtype NOD2 [GeneID=64127]: untreated versus muramyl dipeptide [PubChem=11620162] for 6h.

description_full:
[cell repeats an earlier one in this file: 955 characters]


systematic_name: M8174
exact_source: GSE22611_3840_200_DN
source_species_code: HS
GEO_id: GSE22611
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in HEK293 cells at 2h after stimulation by muramyl dipeptide [PubChem=11620162]: over-expressing mutant NOD2 [GeneID=64127] versus control.

description_full:
[cell repeats an earlier one in this file: 955 characters]


systematic_name: M8175
exact_source: GSE22611_3476_200_DN
source_species_code: HS
GEO_id: GSE22611
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in HEK293 cells expressing mutant NOD2 [GeneID=64127]: untreated versus muramyl dipeptide [PubChem=11620162] for 2h.

description_full:
[cell repeats an earlier one in this file: 955 characters]


systematic_name: M8177
exact_source: GSE22611_3479_200_UP
source_species_code: HS
GEO_id: GSE22611
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in HEK293 cells at 2h after stimulation by muramyl dipeptide [PubChem=11620162]: over-expressing wildtype NOD2 [GeneID=64127] versus control.

description_full:
[cell repeats an earlier one in this file: 955 characters]


systematic_name: M8178
exact_source: GSE22611_3479_200_DN
source_species_code: HS
GEO_id: GSE22611
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in HEK293 cells at 2h after stimulation by muramyl dipeptide [PubChem=11620162]: over-expressing wildtype NOD2 [GeneID=64127] versus control.

description_full:
[cell repeats an earlier one in this file: 955 characters]


systematic_name: M8181
exact_source: GSE25677_1568_200_DN
source_species_code: MM
GEO_id: GSE25677
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in B lymphocytes immunized with: monophosphoryl lipid A (MPL) versus MPL and imiquimod [PubChem=13982876].

description_full:
  Many successful vaccines induce persistent antibody responses that can last a lifetime. The mechanisms by which they do so remain unclear, but emerging evidence suggests that activate dendritic cells (DCs) via Toll-like receptors (TLRs). For example, the yellow fever vaccine YF-17D, one of the most successful empiric vaccines ever developed, activates DCs via multiple TLRs to stimulate pro-inflammatory cytokines. Triggering specific combinations of TLRs in DCs can induce synergistic production of cytokines, which results in enhanced T cell responses, but its impact on antibody responses remain unknown. Learning the critical parameters of innate immunity that programs such antibody responses remains a major challenge in vaccinology. We demonstrated that immunization of mice with synthetic nanoparticles containing antigens plus Toll-like receptor (TLR) ligands 4 (MPL) + 7 (R837) induces synergistic increases in antigen-specific, neutralizing antibodies compared to immunization with a single TLR ligand. To determine whether there was any early programming of B cells, we isolated isotype switched, TCRbeta-CD11b-CD19+IgD-IgG+ B cells by FACS at 7 days post immunization with nanoparticles containing various adjuvants plus OVA, and performed microarray analyses to assess their molecular signatures.


systematic_name: M8182
exact_source: GSE25677_1569_200_DN
source_species_code: MM
GEO_id: GSE25677
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in B lymphocytes immunized with: imiquimod [PubChem=13982876] versus monophosphoryl lipid A and imiquimod [PubChem=13982876].

description_full:
  Many successful vaccines induce persistent antibody responses that can last a lifetime. The mechanisms by which they do so remain unclear, but emerging evidence suggests that activate dendritic cells (DCs) via Toll-like receptors (TLRs). For example, the yellow fever vaccine YF-17D, one of the most successful empiric vaccines ever developed, activates DCs via multiple TLRs to stimulate pro-inflammatory cytokines. Triggering specific combinations of TLRs in DCs can induce synergistic production of cytokines, which results in enhanced T cell responses, but its impact on antibody responses remain unknown. Learning the critical parameters of innate immunity that programs such antibody responses remains a major challenge in vaccinology. We demonstrated that immunization of mice with synthetic nanoparticles containing antigens plus Toll-like receptor (TLR) ligands 4 (MPL) + 7 (R837) induces synergistic increases in antigen-specific, neutralizing antibodies compared to immunization with a single TLR ligand. To determine whether there was any early programming of B cells, we isolated isotype switched, TCRbeta-CD11b-CD19+IgD-IgG+ B cells by FACS at 7 days post immunization with nanoparticles containing various adjuvants plus OVA, and performed microarray analyses to assess their molecular signatures.


systematic_name: M8183
exact_source: GSE25677_1568_200_UP
source_species_code: MM
GEO_id: GSE25677
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in B lymphocytes immunized with: monophosphoryl lipid A (MPL) versus MPL and imiquimod [PubChem=13982876].

description_full:
  Many successful vaccines induce persistent antibody responses that can last a lifetime. The mechanisms by which they do so remain unclear, but emerging evidence suggests that activate dendritic cells (DCs) via Toll-like receptors (TLRs). For example, the yellow fever vaccine YF-17D, one of the most successful empiric vaccines ever developed, activates DCs via multiple TLRs to stimulate pro-inflammatory cytokines. Triggering specific combinations of TLRs in DCs can induce synergistic production of cytokines, which results in enhanced T cell responses, but its impact on antibody responses remain unknown. Learning the critical parameters of innate immunity that programs such antibody responses remains a major challenge in vaccinology. We demonstrated that immunization of mice with synthetic nanoparticles containing antigens plus Toll-like receptor (TLR) ligands 4 (MPL) + 7 (R837) induces synergistic increases in antigen-specific, neutralizing antibodies compared to immunization with a single TLR ligand. To determine whether there was any early programming of B cells, we isolated isotype switched, TCRbeta-CD11b-CD19+IgD-IgG+ B cells by FACS at 7 days post immunization with nanoparticles containing various adjuvants plus OVA, and performed microarray analyses to assess their molecular signatures.


systematic_name: M8185
exact_source: GSE25677_1569_200_UP
source_species_code: MM
GEO_id: GSE25677
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in B lymphocytes immunized with: imiquimod [PubChem=13982876] versus monophosphoryl lipid A and imiquimod [PubChem=13982876].

description_full:
[cell repeats an earlier one in this file: 1312 characters]


systematic_name: M8186
exact_source: GSE25677_1567_200_UP
source_species_code: MM
GEO_id: GSE25677
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in B lymphocytes after immunization with: monophosphoryl lipid A versus imiquimod [PubChem=13982876].

description_full:
[cell repeats an earlier one in this file: 1312 characters]


systematic_name: M8187
exact_source: GSE25677_1567_200_DN
source_species_code: MM
GEO_id: GSE25677
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in B lymphocytes after immunization with: monophosphoryl lipid A versus imiquimod [PubChem=13982876].

description_full:
[cell repeats an earlier one in this file: 1312 characters]


systematic_name: M8188
exact_source: GSE26488_2971_200_DN
source_species_code: MM
GEO_id: GSE26488
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in double positive thymocytes: wildtype versus over-expressing HDAC7[GeneID=51564] fused with VP16.

description_full:
  Abstract of publicaton: CD4/CD8 double-positive (DP) thymocytes express the transcriptional repressor Histone Deacetylase 7 (HDAC7), a class IIa HDAC that is exported from the cell nucleus after T cell receptor (TCR) engagement. Through signal-dependent nuclear export, class IIa HDACs such as HDAC7 mediate signal-dependent changes in gene expression that are important to developmental fate decisions in multiple tissues. We report that HDAC7 is exported from the cell nucleus during positive selection in thymocytes, and regulates genes mediating the coupling between TCR engagement and downstream events that determine cell survival. Thymocytes lacking HDAC7 are inefficiently positively selected due to a severely shortened lifespan and exhibit a truncated repertoire of TCR Jalpha segments. The expression of multiple important mediators and modulators of the response to TCR engagement is altered in HDAC7-deficient thymocytes, resulting in increased tonic MAP kinase activity that contributes to the observed loss of viability. Remarkably, the activity of Protein Kinase D, the kinase that mediates nuclear export of HDAC7 in response to TCR signaling, is also increased in HDAC7-deficient thymocytes, suggesting that HDAC7 nuclear export governs a self-sustaining auto-excitatory loop. These experiments add to the understanding of the life/death decision in thymic T cell development, define a novel function for class IIa HDACs, and point to a novel feed-forward mechanism whereby these molecules regulate their own state and mediate stable developmental transitions. Title of manuscript: Nuclear Export of Histone Deacetylase 7 During Thymic Selection Mediates Immune Self-tolerance. abstract of manuscript: Histone Deacetylase 7 (HDAC7) is a TCR signal-dependent regulator of differentiation that is highly expressed in CD4/CD8 double-positive (DP) thymocytes. Here we examine the effect of blocking TCR-dependent nuclear export of HDAC7 during thymic selection, through expression of a signal-resistant mutant of HDAC7 (HDAC7-delta-P) in thymocytes. We find that HDAC7-delta-P Transgenic thymocytes exhibit a profound block in negative thymic selection, but can still undergo positive selection, resulting in the escape of autoreactive T cells into the periphery. Gene expression profiling reveals a comprehensive suppression of the negative selection-associated gene expression program in DP thymocytes, associated with a defect in the activation of MAP kinase pathways by TCR signals. The consequence of this block in vivo is a lethal autoimmune syndrome involving the exocrine pancreas and other abdominal organs. These experiments establish a novel molecular model of autoimmunity and cast new light on the relationship between thymic selection and immune self-tolerance. Goal of Microarray experiment: We did these experiments to determine how alteration of the function of HDAC7, a site-specific and signal-dependent repressor of transcription, changes gene expression in CD4/CD8 DP thymocytes.


systematic_name: M8189
exact_source: GSE26488_2973_200_DN
source_species_code: MM
GEO_id: GSE26488
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in double positive thymocytes from OT-2 transgenic mice: control versus injected with agonist peptide.

description_full:
  Abstract of publicaton: CD4/CD8 double-positive (DP) thymocytes express the transcriptional repressor Histone Deacetylase 7 (HDAC7), a class IIa HDAC that is exported from the cell nucleus after T cell receptor (TCR) engagement. Through signal-dependent nuclear export, class IIa HDACs such as HDAC7 mediate signal-dependent changes in gene expression that are important to developmental fate decisions in multiple tissues. We report that HDAC7 is exported from the cell nucleus during positive selection in thymocytes, and regulates genes mediating the coupling between TCR engagement and downstream events that determine cell survival. Thymocytes lacking HDAC7 are inefficiently positively selected due to a severely shortened lifespan and exhibit a truncated repertoire of TCR Jalpha segments. The expression of multiple important mediators and modulators of the response to TCR engagement is altered in HDAC7-deficient thymocytes, resulting in increased tonic MAP kinase activity that contributes to the observed loss of viability. Remarkably, the activity of Protein Kinase D, the kinase that mediates nuclear export of HDAC7 in response to TCR signaling, is also increased in HDAC7-deficient thymocytes, suggesting that HDAC7 nuclear export governs a self-sustaining auto-excitatory loop. These experiments add to the understanding of the life/death decision in thymic T cell development, define a novel function for class IIa HDACs, and point to a novel feed-forward mechanism whereby these molecules regulate their own state and mediate stable developmental transitions. Title of manuscript: Nuclear Export of Histone Deacetylase 7 During Thymic Selection Mediates Immune Self-tolerance. abstract of manuscript: Histone Deacetylase 7 (HDAC7) is a TCR signal-dependent regulator of differentiation that is highly expressed in CD4/CD8 double-positive (DP) thymocytes. Here we examine the effect of blocking TCR-dependent nuclear export of HDAC7 during thymic selection, through expression of a signal-resistant mutant of HDAC7 (HDAC7-delta-P) in thymocytes. We find that HDAC7-delta-P Transgenic thymocytes exhibit a profound block in negative thymic selection, but can still undergo positive selection, resulting in the escape of autoreactive T cells into the periphery. Gene expression profiling reveals a comprehensive suppression of the negative selection-associated gene expression program in DP thymocytes, associated with a defect in the activation of MAP kinase pathways by TCR signals. The consequence of this block in vivo is a lethal autoimmune syndrome involving the exocrine pancreas and other abdominal organs. These experiments establish a novel molecular model of autoimmunity and cast new light on the relationship between thymic selection and immune self-tolerance. Goal of Microarray experiment: We did these experiments to determine how alteration of the function of HDAC7, a site-specific and signal-dependent repressor of transcription, changes gene expression in CD4/CD8 DP thymocytes.


systematic_name: M8190
exact_source: GSE26488_2972_200_UP
source_species_code: MM
GEO_id: GSE26488
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in double positive thymocytes: HDAC7 [GeneID=51564] knockout versus over-expressing HDAC7 [GeneID=51564] fused with VP16.

description_full:
  Abstract of publicaton: CD4/CD8 double-positive (DP) thymocytes express the transcriptional repressor Histone Deacetylase 7 (HDAC7), a class IIa HDAC that is exported from the cell nucleus after T cell receptor (TCR) engagement. Through signal-dependent nuclear export, class IIa HDACs such as HDAC7 mediate signal-dependent changes in gene expression that are important to developmental fate decisions in multiple tissues. We report that HDAC7 is exported from the cell nucleus during positive selection in thymocytes, and regulates genes mediating the coupling between TCR engagement and downstream events that determine cell survival. Thymocytes lacking HDAC7 are inefficiently positively selected due to a severely shortened lifespan and exhibit a truncated repertoire of TCR Jalpha segments. The expression of multiple important mediators and modulators of the response to TCR engagement is altered in HDAC7-deficient thymocytes, resulting in increased tonic MAP kinase activity that contributes to the observed loss of viability. Remarkably, the activity of Protein Kinase D, the kinase that mediates nuclear export of HDAC7 in response to TCR signaling, is also increased in HDAC7-deficient thymocytes, suggesting that HDAC7 nuclear export governs a self-sustaining auto-excitatory loop. These experiments add to the understanding of the life/death decision in thymic T cell development, define a novel function for class IIa HDACs, and point to a novel feed-forward mechanism whereby these molecules regulate their own state and mediate stable developmental transitions. Title of manuscript: Nuclear Export of Histone Deacetylase 7 During Thymic Selection Mediates Immune Self-tolerance. abstract of manuscript: Histone Deacetylase 7 (HDAC7) is a TCR signal-dependent regulator of differentiation that is highly expressed in CD4/CD8 double-positive (DP) thymocytes. Here we examine the effect of blocking TCR-dependent nuclear export of HDAC7 during thymic selection, through expression of a signal-resistant mutant of HDAC7 (HDAC7-delta-P) in thymocytes. We find that HDAC7-delta-P Transgenic thymocytes exhibit a profound block in negative thymic selection, but can still undergo positive selection, resulting in the escape of autoreactive T cells into the periphery. Gene expression profiling reveals a comprehensive suppression of the negative selection-associated gene expression program in DP thymocytes, associated with a defect in the activation of MAP kinase pathways by TCR signals. The consequence of this block in vivo is a lethal autoimmune syndrome involving the exocrine pancreas and other abdominal organs. These experiments establish a novel molecular model of autoimmunity and cast new light on the relationship between thymic selection and immune self-tolerance. Goal of Microarray experiment: We did these experiments to determine how alteration of the function of HDAC7, a site-specific and signal-dependent repressor of transcription, changes gene expression in CD4/CD8 DP thymocytes.


systematic_name: M8193
exact_source: GSE26488_2973_200_UP
source_species_code: MM
GEO_id: GSE26488
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in double positive thymocytes from OT-2 transgenic mice: control versus injected with agonist peptide.

description_full:
[cell repeats an earlier one in this file: 3014 characters]


systematic_name: M8196
exact_source: GSE26488_2972_200_DN
source_species_code: MM
GEO_id: GSE26488
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in double positive thymocytes: HDAC7 [GeneID=51564] knockout versus over-expressing HDAC7 [GeneID=51564] fused with VP16.

description_full:
[cell repeats an earlier one in this file: 3014 characters]


systematic_name: M8197
exact_source: GSE26488_2975_200_DN
source_species_code: MM
GEO_id: GSE26488
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in dobule positive thymocytefrom OT-2 transgenic mice injected with agonist peptide: wildtype versus expressing deltaP form of HDAC7 [GeneID=51564].

description_full:
[cell repeats an earlier one in this file: 3014 characters]


systematic_name: M8198
exact_source: GSE26488_2975_200_UP
source_species_code: MM
GEO_id: GSE26488
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in dobule positive thymocytefrom OT-2 transgenic mice injected with agonist peptide: wildtype versus expressing deltaP form of HDAC7 [GeneID=51564].

description_full:
[cell repeats an earlier one in this file: 3014 characters]


systematic_name: M8199
exact_source: GSE26488_2974_200_DN
source_species_code: MM
GEO_id: GSE26488
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in double positive thymocyte from OT-2 transgenic mice: control versus HDAC7 [GeneID=51564] deltaP form after injection with agonist peptide.

description_full:
[cell repeats an earlier one in this file: 3014 characters]


systematic_name: M8200
exact_source: GSE26488_2971_200_UP
source_species_code: MM
GEO_id: GSE26488
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in double positive thymocytes: wildtype versus over-expressing HDAC7[GeneID=51564] fused with VP16.

description_full:
[cell repeats an earlier one in this file: 3014 characters]


systematic_name: M8201
exact_source: GSE26488_2974_200_UP
source_species_code: MM
GEO_id: GSE26488
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in double positive thymocyte from OT-2 transgenic mice: control versus HDAC7 [GeneID=51564] deltaP form after injection with agonist peptide.

description_full:
[cell repeats an earlier one in this file: 3014 characters]


systematic_name: M8203
exact_source: GSE27092_2642_200_UP
source_species_code: MM
GEO_id: GSE27092
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in wildtype cytotoxic T lymphocytes versus those overexpressing phosphorylation deficient form of HDAC7 [GeneID=51564].

description_full:
  The present study reports an unbiased analysis of the cytotoxic T cell serine-threonine phosphoproteome using high resolution mass spectrometry. Approximately 2,000 phosphorylations were identified in CTLs of which approximately 450 were controlled by TCR signaling. A significantly overrepresented group of molecules identified in the phosphoproteomic screen were transcription activators, co-repressors and chromatin regulators. A focus on the chromatin regulators revealed that CTLs have high expression of the histone deacetylase HDAC7 but continually phosphorylate and export this transcriptional repressor from the nucleus. HDAC7 dephosphorylation results in its nuclear accumulation and suppressed expression of genes encoding key cytokines, cytokine receptors and adhesion molecules that determine CTL function. The screening of the CTL phosphoproteome thus reveals intrinsic pathways of serine-threonine phosphorylation that target chromatin regulators in CTLs and determine the CTL functional program. We used Affymetrix microarray analysis to explore the molecular basis for the role of HDAC7 in CTLs and the impact of GFP-HDAC7 phosphorylation deficient mutant expression on the CTL transcriptional profile.


systematic_name: M8204
exact_source: GSE27092_2642_200_DN
source_species_code: MM
GEO_id: GSE27092
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in wildtype cytotoxic T lymphocytes versus those overexpressing phosphorylation deficient form of HDAC7 [GeneID=51564].

description_full:
  The present study reports an unbiased analysis of the cytotoxic T cell serine-threonine phosphoproteome using high resolution mass spectrometry. Approximately 2,000 phosphorylations were identified in CTLs of which approximately 450 were controlled by TCR signaling. A significantly overrepresented group of molecules identified in the phosphoproteomic screen were transcription activators, co-repressors and chromatin regulators. A focus on the chromatin regulators revealed that CTLs have high expression of the histone deacetylase HDAC7 but continually phosphorylate and export this transcriptional repressor from the nucleus. HDAC7 dephosphorylation results in its nuclear accumulation and suppressed expression of genes encoding key cytokines, cytokine receptors and adhesion molecules that determine CTL function. The screening of the CTL phosphoproteome thus reveals intrinsic pathways of serine-threonine phosphorylation that target chromatin regulators in CTLs and determine the CTL functional program. We used Affymetrix microarray analysis to explore the molecular basis for the role of HDAC7 in CTLs and the impact of GFP-HDAC7 phosphorylation deficient mutant expression on the CTL transcriptional profile.


description_brief: Genes up-regulated in macrophages: tumoricidal versus control.
systematic_name: M8205
exact_source: GSE26912_3062_200_UP
source_species_code: MM
GEO_id: GSE26912
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  The immune system can both promote and suppress cancer. Chronic inflammation and proinflammatory cytokines such as interleukin (IL)-1 and IL-6 are considered tumor-promoting. In contrast, the exact nature of protective antitumor immunity remains obscure. In this study, we have quantified locally secreted cytokines during primary immune responses against myeloma and B-cell lymphoma in mice. Strikingly, successful cancer immunosurveillance mediated by tumor-specific CD4+ T cells was consistently associated with elevated local levels of both proinflammatory (IL-1aplha, IL-1beta, and IL-6) and T helper 1 (Th1)-associated cytokines (interferon-alpha, IL-2, IL-12). Cancer eradication was achieved by a collaboration between tumor-specific Th1 cells and tumor-infiltrating, antigen-presenting macrophages. Th1 cells induced secretion of IL-1-beta and IL-6 by macrophages. Th1-derived interferon-gamma was shown to render macrophages directly cytotoxic to cancer cells, and to induce macrophages to secrete the angiostatic chemokines CXCL9/MIG and CXCL10/IP-10. Thus, inflammation, when driven by tumor-specific Th1 cells, may prevent rather than promote cancer.


systematic_name: M8208
exact_source: GSE27670_3494_200_DN
source_species_code: HS
GEO_id: GSE27670
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in germinal center B lymphocytes: control versus over-expressing PRDM1 [GeneID=639].

description_full:
  In this study, we have investigated the effect of BLIMP1α on gene expression, cell differentiation and pathogenesis in normal human GC B cells using a non-viral vector based system


systematic_name: M8209
exact_source: GSE27670_3496_200_UP
source_species_code: HS
GEO_id: GSE27670
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in germinal center B lymphocytes over-expressing: PRDM1 [GeneID=639] versus Epstein-Barr virus protein LMP1.

description_full:
  In this study, we have investigated the effect of BLIMP1α on gene expression, cell differentiation and pathogenesis in normal human GC B cells using a non-viral vector based system


systematic_name: M8211
exact_source: GSE27670_3496_200_DN
source_species_code: HS
GEO_id: GSE27670
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in germinal center B lymphocytes over-expressing: PRDM1 [GeneID=639] versus Epstein-Barr virus protein LMP1.

description_full:
  In this study, we have investigated the effect of BLIMP1α on gene expression, cell differentiation and pathogenesis in normal human GC B cells using a non-viral vector based system


systematic_name: M8212
exact_source: GSE27670_3494_200_UP
source_species_code: HS
GEO_id: GSE27670
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in germinal center B lymphocytes: control versus over-expressing PRDM1 [GeneID=639].

description_full:
[cell repeats an earlier one in this file: 180 characters]


systematic_name: M8216
exact_source: GSE27670_3495_200_UP
source_species_code: HS
GEO_id: GSE27670
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in germinal center B lymphocytes: control versus over-expressing Epstein-Barr virus protein LMP1.

description_full:
[cell repeats an earlier one in this file: 180 characters]


systematic_name: M8217
exact_source: GSE27670_3495_200_DN
source_species_code: HS
GEO_id: GSE27670
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in germinal center B lymphocytes: control versus over-expressing Epstein-Barr virus protein LMP1.

description_full:
[cell repeats an earlier one in this file: 180 characters]


systematic_name: M8218
exact_source: GSE22443_2729_200_DN
source_species_code: MM
GEO_id: GSE22443
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in Pmel-1 CD8 T cells primed with cognate antigen: IL2 [GeneID=3558] versus IL-12.

description_full:
  The expansion, trafficking and functional effectiveness of adoptively transferred CD8+ T-cells play a critical role in mediating effective anti-tumor immunity. However, the mechanisms which program the highly proliferative and functional state of CD8+ T-cells are not completely understood. We hypothesized that IL-12, a cytokine commonly induced by TLR activation, could enhance T-cell priming by altering responsiveness to antigen and cytokines. Priming of tumor specific CD8+ T-cells in the presence of IL-12 induced the acquisition of a 'polyfunctional' effector response and increased the generation of memory cells. Moreover, IL-12 priming also promoted high levels of the IL-2 receptor alpha-chain (CD25) and robust IL-2 mediated activation of STAT5. This sensitivity to IL-2 translated into enhanced in vivo proliferation of adoptively transferred CD8+ T-cells. Furthermore, real-time, in vivo imaging of T-cell trafficking confirmed the ability of IL-12 priming to drive in vivo proliferation. IL-12 priming enhanced the anti-tumor function of adoptively transferred cells by reducing established subcutaneous tumor burden, and significantly increasing survival in an established intracranial tumor model. Finally, IL-12 priming of human PBMCs generates tumor specific T-cells phenotypically and functionally similar to IL-12 primed Pmel-1 T-cells. These results highlight IL-12 as an important mediator of CD8+ T-cell effector function and anti-tumor immunity.


systematic_name: M8220
exact_source: GSE22443_2727_200_DN
source_species_code: MM
GEO_id: GSE22443
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in Pmel-1 CD8 T cells: naïve versus primed with cognate antigen (gp100) and IL2 [GeneID=3558].

description_full:
  The expansion, trafficking and functional effectiveness of adoptively transferred CD8+ T-cells play a critical role in mediating effective anti-tumor immunity. However, the mechanisms which program the highly proliferative and functional state of CD8+ T-cells are not completely understood. We hypothesized that IL-12, a cytokine commonly induced by TLR activation, could enhance T-cell priming by altering responsiveness to antigen and cytokines. Priming of tumor specific CD8+ T-cells in the presence of IL-12 induced the acquisition of a 'polyfunctional' effector response and increased the generation of memory cells. Moreover, IL-12 priming also promoted high levels of the IL-2 receptor alpha-chain (CD25) and robust IL-2 mediated activation of STAT5. This sensitivity to IL-2 translated into enhanced in vivo proliferation of adoptively transferred CD8+ T-cells. Furthermore, real-time, in vivo imaging of T-cell trafficking confirmed the ability of IL-12 priming to drive in vivo proliferation. IL-12 priming enhanced the anti-tumor function of adoptively transferred cells by reducing established subcutaneous tumor burden, and significantly increasing survival in an established intracranial tumor model. Finally, IL-12 priming of human PBMCs generates tumor specific T-cells phenotypically and functionally similar to IL-12 primed Pmel-1 T-cells. These results highlight IL-12 as an important mediator of CD8+ T-cell effector function and anti-tumor immunity.


systematic_name: M8221
exact_source: GSE22443_2728_200_UP
source_species_code: MM
GEO_id: GSE22443
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in Pmel-1 CD8 T cells: naïve versus primed with cognate antigen (gp100) and IL-12.

description_full:
  The expansion, trafficking and functional effectiveness of adoptively transferred CD8+ T-cells play a critical role in mediating effective anti-tumor immunity. However, the mechanisms which program the highly proliferative and functional state of CD8+ T-cells are not completely understood. We hypothesized that IL-12, a cytokine commonly induced by TLR activation, could enhance T-cell priming by altering responsiveness to antigen and cytokines. Priming of tumor specific CD8+ T-cells in the presence of IL-12 induced the acquisition of a 'polyfunctional' effector response and increased the generation of memory cells. Moreover, IL-12 priming also promoted high levels of the IL-2 receptor alpha-chain (CD25) and robust IL-2 mediated activation of STAT5. This sensitivity to IL-2 translated into enhanced in vivo proliferation of adoptively transferred CD8+ T-cells. Furthermore, real-time, in vivo imaging of T-cell trafficking confirmed the ability of IL-12 priming to drive in vivo proliferation. IL-12 priming enhanced the anti-tumor function of adoptively transferred cells by reducing established subcutaneous tumor burden, and significantly increasing survival in an established intracranial tumor model. Finally, IL-12 priming of human PBMCs generates tumor specific T-cells phenotypically and functionally similar to IL-12 primed Pmel-1 T-cells. These results highlight IL-12 as an important mediator of CD8+ T-cell effector function and anti-tumor immunity.


systematic_name: M8222
exact_source: GSE22443_2727_200_UP
source_species_code: MM
GEO_id: GSE22443
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in Pmel-1 CD8 T cells: naïve versus primed with cognate antigen (gp100) and IL2 [GeneID=3558].

description_full:
[cell repeats an earlier one in this file: 1470 characters]


systematic_name: M8223
exact_source: GSE22443_2729_200_UP
source_species_code: MM
GEO_id: GSE22443
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in Pmel-1 CD8 T cells primed with cognate antigen: IL2 [GeneID=3558] versus IL-12.

description_full:
[cell repeats an earlier one in this file: 1470 characters]


systematic_name: M8225
exact_source: GSE22443_2728_200_DN
source_species_code: MM
GEO_id: GSE22443
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in Pmel-1 CD8 T cells: naïve versus primed with cognate antigen (gp100) and IL-12.

description_full:
[cell repeats an earlier one in this file: 1470 characters]


systematic_name: M8226
exact_source: GSE27241_2894_200_UP
source_species_code: MM
GEO_id: GSE27241
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in polarizing CD4 [GeneID=920] Th17 cells: wildtype untreated versus RORC [GeneID=6097] knockout treated by digoxin [PubChem=2724385].

description_full:
  CD4+ T helper lymphocytes that express interleukin-17 (Th17 cells) have critical roles in mouse models of autoimmunity, and there is mounting evidence that they also influence inflammatory processes in humans. Genome-wide association studies in humans have linked genes involved in Th17 cell differentiation and function with susceptibility to Crohn’s disease, rheumatoid arthritis, and psoriasis1-3. Thus, the pathway towards differentiation of Th17 cells and, perhaps, of related innate lymphoid cells with similar effector functions4, 5, is an attractive target for therapeutic applications. Mouse and human Th17 cells are distinguished by expression of the retinoic acid receptor-related orphan nuclear receptor RORγt, which is required for induction of IL-17 transcription and for the manifestation of Th17-dependent autoimmune disease in mice6. By performing a chemical screen with an insect cell-based reporter system, we identified the cardiac glycoside digoxin as a specific inhibitor of RORγt transcriptional activity. Digoxin inhibited murine Th17 cell differentiation without affecting differentiation of other T cell lineages and was effective in delaying the onset and reducing the severity of autoimmune disease in mice. At high concentrations, digoxin is toxic for human cells, but non-toxic synthetic derivatives, 20,22-dihydrodigoxin-21,23-diol (Dig(dhd)) and digoxin-21-salicylidene (Dig(sal)), specifically inhibited induction of IL-17 in human CD4+ T cells. Using these small molecule compounds, we demonstrated that RORγt is imporant for the maintenance of IL-17 expression in mouse and human effector T cells. These data suggest that derivatives of digoxin can be used as chemical probes for development of RORγt-targeted therapeutic agents that attenuate inflammatory lymphocyte function and autoimmune disease.


systematic_name: M8227
exact_source: GSE27241_2892_200_DN
source_species_code: MM
GEO_id: GSE27241
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in polarizing CD4 [GeneID=920] Th17 cells: untreated versus digoxin [PubChem=2724385].

description_full:
  CD4+ T helper lymphocytes that express interleukin-17 (Th17 cells) have critical roles in mouse models of autoimmunity, and there is mounting evidence that they also influence inflammatory processes in humans. Genome-wide association studies in humans have linked genes involved in Th17 cell differentiation and function with susceptibility to Crohn’s disease, rheumatoid arthritis, and psoriasis1-3. Thus, the pathway towards differentiation of Th17 cells and, perhaps, of related innate lymphoid cells with similar effector functions4, 5, is an attractive target for therapeutic applications. Mouse and human Th17 cells are distinguished by expression of the retinoic acid receptor-related orphan nuclear receptor RORγt, which is required for induction of IL-17 transcription and for the manifestation of Th17-dependent autoimmune disease in mice6. By performing a chemical screen with an insect cell-based reporter system, we identified the cardiac glycoside digoxin as a specific inhibitor of RORγt transcriptional activity. Digoxin inhibited murine Th17 cell differentiation without affecting differentiation of other T cell lineages and was effective in delaying the onset and reducing the severity of autoimmune disease in mice. At high concentrations, digoxin is toxic for human cells, but non-toxic synthetic derivatives, 20,22-dihydrodigoxin-21,23-diol (Dig(dhd)) and digoxin-21-salicylidene (Dig(sal)), specifically inhibited induction of IL-17 in human CD4+ T cells. Using these small molecule compounds, we demonstrated that RORγt is imporant for the maintenance of IL-17 expression in mouse and human effector T cells. These data suggest that derivatives of digoxin can be used as chemical probes for development of RORγt-targeted therapeutic agents that attenuate inflammatory lymphocyte function and autoimmune disease.


systematic_name: M8233
exact_source: GSE27241_2895_200_DN
source_species_code: MM
GEO_id: GSE27241
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in polarizing CD4 [GeneID=920] Th17 cells treated by digoxin [PubChem=2724385]: wildtype versus RORC [GeneID=6097] knockout.

description_full:
  CD4+ T helper lymphocytes that express interleukin-17 (Th17 cells) have critical roles in mouse models of autoimmunity, and there is mounting evidence that they also influence inflammatory processes in humans. Genome-wide association studies in humans have linked genes involved in Th17 cell differentiation and function with susceptibility to Crohn’s disease, rheumatoid arthritis, and psoriasis1-3. Thus, the pathway towards differentiation of Th17 cells and, perhaps, of related innate lymphoid cells with similar effector functions4, 5, is an attractive target for therapeutic applications. Mouse and human Th17 cells are distinguished by expression of the retinoic acid receptor-related orphan nuclear receptor RORγt, which is required for induction of IL-17 transcription and for the manifestation of Th17-dependent autoimmune disease in mice6. By performing a chemical screen with an insect cell-based reporter system, we identified the cardiac glycoside digoxin as a specific inhibitor of RORγt transcriptional activity. Digoxin inhibited murine Th17 cell differentiation without affecting differentiation of other T cell lineages and was effective in delaying the onset and reducing the severity of autoimmune disease in mice. At high concentrations, digoxin is toxic for human cells, but non-toxic synthetic derivatives, 20,22-dihydrodigoxin-21,23-diol (Dig(dhd)) and digoxin-21-salicylidene (Dig(sal)), specifically inhibited induction of IL-17 in human CD4+ T cells. Using these small molecule compounds, we demonstrated that RORγt is imporant for the maintenance of IL-17 expression in mouse and human effector T cells. These data suggest that derivatives of digoxin can be used as chemical probes for development of RORγt-targeted therapeutic agents that attenuate inflammatory lymphocyte function and autoimmune disease.


systematic_name: M8234
exact_source: GSE27241_2893_200_UP
source_species_code: MM
GEO_id: GSE27241
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in polarizing CD4 [GeneID=920] Th17 cells: wildtype vs RORC [GeneID=6097] knockout treated with digoxin [PubChem=2724385].

description_full:
[cell repeats an earlier one in this file: 1835 characters]


systematic_name: M8235
exact_source: GSE27241_2891_200_UP
source_species_code: MM
GEO_id: GSE27241
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in polarizing CD4 [GeneID=920] Th17 cells: wildtype versus RORC [GeneID=6097] knockout.

description_full:
[cell repeats an earlier one in this file: 1835 characters]


systematic_name: M8238
exact_source: GSE27241_2894_200_DN
source_species_code: MM
GEO_id: GSE27241
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in polarizing CD4 [GeneID=920] Th17 cells: wildtype untreated versus RORC [GeneID=6097] knockout treated by digoxin [PubChem=2724385].

description_full:
[cell repeats an earlier one in this file: 1835 characters]


systematic_name: M8239
exact_source: GSE27241_2895_200_UP
source_species_code: MM
GEO_id: GSE27241
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in polarizing CD4 [GeneID=920] Th17 cells treated by digoxin [PubChem=2724385]: wildtype versus RORC [GeneID=6097] knockout.

description_full:
[cell repeats an earlier one in this file: 1835 characters]


systematic_name: M8241
exact_source: GSE27241_2893_200_DN
source_species_code: MM
GEO_id: GSE27241
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in polarizing CD4 [GeneID=920] Th17 cells: wildtype vs RORC [GeneID=6097] knockout treated with digoxin [PubChem=2724385].

description_full:
[cell repeats an earlier one in this file: 1835 characters]


systematic_name: M8242
exact_source: GSE27241_2891_200_DN
source_species_code: MM
GEO_id: GSE27241
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in polarizing CD4 [GeneID=920] Th17 cells: wildtype versus RORC [GeneID=6097] knockout.

description_full:
[cell repeats an earlier one in this file: 1835 characters]


systematic_name: M8243
exact_source: GSE27241_2892_200_UP
source_species_code: MM
GEO_id: GSE27241
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in polarizing CD4 [GeneID=920] Th17 cells: untreated versus digoxin [PubChem=2724385].

description_full:
[cell repeats an earlier one in this file: 1835 characters]


description_brief: Genes down-regulated in T reg: HDAC6 [GeneID=10013] knockout versus wildtype.
systematic_name: M8246
exact_source: GSE27896_3342_200_DN
source_species_code: MM
GEO_id: GSE27896
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  Foxp3+ T-regulatory cells (Tregs) are key to immune homeostasis such that their diminished numbers or function can cause autoimmunity and allograft rejection. Foxp3+ Tregs express histone/protein deacetylases (HDACs) that regulate chromatin remodeling, gene expression and protein function. Pan-HDAC inhibitors developed for oncology enhance Treg production and suppression but have limited non-oncologic applications given their broad effects. We show, using HDAC6-deficient mice and WT mice treated with HDAC6-specific inhibitors, that HDAC6 inhibition promotes Treg suppressive activity in models of inflammation and autoimmunity, including multiple forms of experimental colitis and fully MHC-incompatible cardiac allograft rejection. Many of the beneficial effects of HDAC6 targeting are also achieved by inhibition of the HDAC6-regulated protein, HSP90. Hence, selective targeting of a single HDAC isoform, HDAC6, or its downstream target, HSP90, can promote Treg-dependent suppression of autoimmunity and transplant rejection.


description_brief: Genes up-regulated in B lymphocytes: control versus stimulated by anti-IgM for 8h.
systematic_name: M8249
exact_source: GSE21063_3433_200_UP
source_species_code: MM
GEO_id: GSE21063
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  Triggering of B cell receptors (BCR) induces a massive synthesis of NFATc1 in splenic B cells. By inactivating the Nfatc1 gene and re-expressing NFATc1 we show that NFATc1 levels are critical for the survival of splenic B cells upon BCR stimulation. NFATc1 ablation led to decreased BCR-induced Ca++ flux and proliferation of splenic B cells, increased apoptosis and suppressed germinal centre formation and immunoglobulin class switch by T cell-independent antigens. By controlling IL-10 synthesis in B cells, NFATc1 supported the proliferation and IL-2 synthesis of T cells in vitro and appeared to contribute to the mild clinical course of Experimental Autoimmune Encephalomyelitis in mice bearing NFATc1-/- B cells. These data indicate NFATc1 as a key factor controlling B cell function.


systematic_name: M8252
exact_source: GSE21063_3441_200_DN
source_species_code: MM
GEO_id: GSE21063
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in B lymphocytes stimulated by anti-IgM for 16h: wildtype versus NFATC1 [GeneID=4772] knockout.

description_full:
[cell repeats an earlier one in this file: 791 characters]


systematic_name: M8253
exact_source: GSE21063_3439_200_DN
source_species_code: MM
GEO_id: GSE21063
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in B lymphocytes stimulated by anti-IgM for 3h: wildtype versus NFATC1 [GeneID=4772] knockout.

description_full:
[cell repeats an earlier one in this file: 791 characters]


systematic_name: M8255
exact_source: GSE21063_3443_200_UP
source_species_code: MM
GEO_id: GSE21063
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in B lymphocytes with NFATC1 [GeneID=4772] knockout stimulated by anti-IgM: 3h versus 16h.

description_full:
[cell repeats an earlier one in this file: 791 characters]


systematic_name: M8257
exact_source: GSE21063_3443_200_DN
source_species_code: MM
GEO_id: GSE21063
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in B lymphocytes with NFATC1 [GeneID=4772] knockout stimulated by anti-IgM: 3h versus 16h.

description_full:
[cell repeats an earlier one in this file: 791 characters]


systematic_name: M8258
exact_source: GSE21063_3437_200_UP
source_species_code: MM
GEO_id: GSE21063
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in B lymphocytes with NFATC1 [GeneID=4772] knockout: control versus stimulated by anti-IgM for 16h.

description_full:
[cell repeats an earlier one in this file: 791 characters]


systematic_name: M8259
exact_source: GSE21063_3437_200_DN
source_species_code: MM
GEO_id: GSE21063
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in B lymphocytes with NFATC1 [GeneID=4772] knockout: control versus stimulated by anti-IgM for 16h.

description_full:
[cell repeats an earlier one in this file: 791 characters]


systematic_name: M8263
exact_source: GSE21063_3439_200_UP
source_species_code: MM
GEO_id: GSE21063
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in B lymphocytes stimulated by anti-IgM for 3h: wildtype versus NFATC1 [GeneID=4772] knockout.

description_full:
[cell repeats an earlier one in this file: 791 characters]


systematic_name: M8269
exact_source: GSE21063_3441_200_UP
source_species_code: MM
GEO_id: GSE21063
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in B lymphocytes stimulated by anti-IgM for 16h: wildtype versus NFATC1 [GeneID=4772] knockout.

description_full:
[cell repeats an earlier one in this file: 791 characters]


systematic_name: M8272
exact_source: GSE21063_3436_200_UP
source_species_code: MM
GEO_id: GSE21063
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in B lymphocytes with NFATC1 [GeneID=4772] knockout: control versus stimulated by anti-IgM for 8h.

description_full:
[cell repeats an earlier one in this file: 791 characters]


systematic_name: M8274
exact_source: GSE21063_3436_200_DN
source_species_code: MM
GEO_id: GSE21063
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in B lymphocytes with NFATC1 [GeneID=4772] knockout: control versus stimulated by anti-IgM for 8h.

description_full:
[cell repeats an earlier one in this file: 791 characters]


systematic_name: M8275
exact_source: GSE21063_3435_200_DN
source_species_code: MM
GEO_id: GSE21063
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in B lymphocytes with NFATC1 [GeneID=4772] knockout: control versus stimulated by anti-IgM for 3h.

description_full:
[cell repeats an earlier one in this file: 791 characters]


systematic_name: M8277
exact_source: GSE21063_3440_200_UP
source_species_code: MM
GEO_id: GSE21063
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in B lymphocytes stimulated by anti-IgM for 8h: wildtype versus NFATC1 [GeneID=4772] knockout.

description_full:
[cell repeats an earlier one in this file: 791 characters]


systematic_name: M8278
exact_source: GSE21063_3440_200_DN
source_species_code: MM
GEO_id: GSE21063
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in B lymphocytes stimulated by anti-IgM for 8h: wildtype versus NFATC1 [GeneID=4772] knockout.

description_full:
[cell repeats an earlier one in this file: 791 characters]


systematic_name: M8279
exact_source: GSE21063_3435_200_UP
source_species_code: MM
GEO_id: GSE21063
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in B lymphocytes with NFATC1 [GeneID=4772] knockout: control versus stimulated by anti-IgM for 3h.

description_full:
[cell repeats an earlier one in this file: 791 characters]


description_brief: Genes up-regulated in thymic memory like CD8 cells: wildtype versus KFL13 [GeneID=51621] knockout.
systematic_name: M8282
exact_source: GSE25502_2482_200_UP
source_species_code: MM
GEO_id: GSE25502
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  “Memory-like T cells” are a subset of thymic cells that acquire effector function through the maturation process rather than interaction with specific antigen. Disruption of genes encoding T cell signaling proteins or transcription factors have provided insights into the differentiation of such cells. We show here that in BALB/c but not C57BL/6 mice, a large portion of thymic CD4-CD8+ T cells exhibit a memory-like phenotype. In BALB/c mice, IL-4 secreted by invariant natural killer T (iNKT) cells is both essential and sufficient for the generation of memory-like T cells. In C57BL/6 mice, iNKT cells are less abundant, producing IL-4 that is insufficient to induce thymic memory-like CD8+ T cells. BALB/c mice deficient in the transcription factor Kruppel-like factor (KLF) 13 have comparable numbers of iNKT cells to C57BL/6 mice and extremely low levels of thymic memory-like CD8+ T cells. This work documents the dramatic impact of a small number of KLF13-dependent iNKT cells.


systematic_name: M8283
exact_source: GSE25502_2482_200_DN
source_species_code: MM
GEO_id: GSE25502
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in thymic memory like CD8 cells: wildtype versus KFL13 [GeneID=51621] knockout.

description_full:
  “Memory-like T cells” are a subset of thymic cells that acquire effector function through the maturation process rather than interaction with specific antigen. Disruption of genes encoding T cell signaling proteins or transcription factors have provided insights into the differentiation of such cells. We show here that in BALB/c but not C57BL/6 mice, a large portion of thymic CD4-CD8+ T cells exhibit a memory-like phenotype. In BALB/c mice, IL-4 secreted by invariant natural killer T (iNKT) cells is both essential and sufficient for the generation of memory-like T cells. In C57BL/6 mice, iNKT cells are less abundant, producing IL-4 that is insufficient to induce thymic memory-like CD8+ T cells. BALB/c mice deficient in the transcription factor Kruppel-like factor (KLF) 13 have comparable numbers of iNKT cells to C57BL/6 mice and extremely low levels of thymic memory-like CD8+ T cells. This work documents the dramatic impact of a small number of KLF13-dependent iNKT cells.


systematic_name: M8284
exact_source: GSE23114_3028_200_UP
source_species_code: MM
GEO_id: GSE23114
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in peritoneal cavity B lymphocytes: wildtype versus lupus susceptibility locus Sle2c1.

description_full:
  Sle2c1 is an NZM2410-derived lupus susceptibility locus that induces an expansion of the B1a cell compartment. B1a cells have a repertoire enriched for autoreactivity, and an expansion of this B cell subset occurs in several mouse models of lupus. Here we showed that expression of Sle2c1 enhances NZB cellular phenotypes that have been associated with autoimmune pathogenesis. A combination of genetic mapping and candidate gene analysis presents Cdkn2c, a gene encoding for cyclin kinase inhibitor p18INK4c (p18), as the top candidate gene for inducing the Slec2c1 associated expansion of B1a cells. A novel SNP in the Cdkn2c promoter is associated with a significantly reduced Cdkn2c expression in the splenic B cells and B1a cells from Sle2c1-carrying mice, which leads to defective G1 cell cycle arrest in splenic B cells and increased proliferation of Pc B1a cells. As cell cycle is differentially regulated in B1a and B2 cells, these results suggest that Cdkn2c play a critical role in B1a cell self renewal, and that its impaired expression leads to an accumulation of these cells with high autoreactive potential.


systematic_name: M8285
exact_source: GSE23114_3028_200_DN
source_species_code: MM
GEO_id: GSE23114
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in peritoneal cavity B lymphocytes: wildtype versus lupus susceptibility locus Sle2c1.

description_full:
  Sle2c1 is an NZM2410-derived lupus susceptibility locus that induces an expansion of the B1a cell compartment. B1a cells have a repertoire enriched for autoreactivity, and an expansion of this B cell subset occurs in several mouse models of lupus. Here we showed that expression of Sle2c1 enhances NZB cellular phenotypes that have been associated with autoimmune pathogenesis. A combination of genetic mapping and candidate gene analysis presents Cdkn2c, a gene encoding for cyclin kinase inhibitor p18INK4c (p18), as the top candidate gene for inducing the Slec2c1 associated expansion of B1a cells. A novel SNP in the Cdkn2c promoter is associated with a significantly reduced Cdkn2c expression in the splenic B cells and B1a cells from Sle2c1-carrying mice, which leads to defective G1 cell cycle arrest in splenic B cells and increased proliferation of Pc B1a cells. As cell cycle is differentially regulated in B1a and B2 cells, these results suggest that Cdkn2c play a critical role in B1a cell self renewal, and that its impaired expression leads to an accumulation of these cells with high autoreactive potential.


systematic_name: M8288
exact_source: GSE23114_3031_200_DN
source_species_code: MM
GEO_id: GSE23114
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in lupus susceptibility locus Sle2c1 B lymphocytes from: peritoneal cavity versus spleen.

description_full:
[cell repeats an earlier one in this file: 1122 characters]


systematic_name: M8294
exact_source: GSE23114_3031_200_UP
source_species_code: MM
GEO_id: GSE23114
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in lupus susceptibility locus Sle2c1 B lymphocytes from: peritoneal cavity versus spleen.

description_full:
[cell repeats an earlier one in this file: 1122 characters]


systematic_name: M8301
exact_source: GSE26727_2449_200_UP
source_species_code: MM
GEO_id: GSE26727
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in peritoneal macrophages treated with LPS: wildtype versus KLF2 [GeneID=10365] knockout.

description_full:
  Gene expression profile of LysMCre/Cre and KLF2∆/∆ primary peritoneal macrophages following 6 hours of LPS treatment. We used microarrays to detail the global program of gene expression following LPS stimulation of LysMCre/Cre and KLF2∆/∆ primary peritoneal macrophages. We identified distinct classes of genes that were altered following LPS stimulation.


systematic_name: M8302
exact_source: GSE26727_2449_200_DN
source_species_code: MM
GEO_id: GSE26727
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in peritoneal macrophages treated with LPS: wildtype versus KLF2 [GeneID=10365] knockout.

description_full:
  Gene expression profile of LysMCre/Cre and KLF2∆/∆ primary peritoneal macrophages following 6 hours of LPS treatment. We used microarrays to detail the global program of gene expression following LPS stimulation of LysMCre/Cre and KLF2∆/∆ primary peritoneal macrophages. We identified distinct classes of genes that were altered following LPS stimulation.


description_brief: Genes down-regulated in naïve T cells: CD4 [GeneID=920] versus Va24- NKT.
systematic_name: M8303
exact_source: GSE28726_3366_200_DN
source_species_code: HS
GEO_id: GSE28726
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  Microarray analysis was performed to determine the transcriptional profiles of NKT, CD1d-aGC+ Va24-, and CD4 T cells.


systematic_name: M8324
exact_source: GSE24574_2337_200_UP
source_species_code: MM
GEO_id: GSE24574
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in follicular helper T cells: BCL6 [GeneID=604] high versus BCL6 [GeneID=604] low.

description_full:
  We found that a number of Tfh cells downmodulated BCL6 protein after their development, and we sought to compare the gene expression between BCL6-hi Tfh cells and BCL6-low Tfh cells.


systematic_name: M8325
exact_source: GSE24574_2337_200_DN
source_species_code: MM
GEO_id: GSE24574
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in follicular helper T cells: BCL6 [GeneID=604] high versus BCL6 [GeneID=604] low.

description_full:
  We found that a number of Tfh cells downmodulated BCL6 protein after their development, and we sought to compare the gene expression between BCL6-hi Tfh cells and BCL6-low Tfh cells.


systematic_name: M8326
exact_source: GSE24574_2338_200_UP
source_species_code: MM
GEO_id: GSE24574
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in BCL6 [GeneID=604] high follicular helper T cells versus naïve T CD4 [GeneID=920] cells.

description_full:
  We found that a number of Tfh cells downmodulated BCL6 protein after their development, and we sought to compare the gene expression between BCL6-hi Tfh cells and BCL6-low Tfh cells.


systematic_name: M8327
exact_source: GSE24574_2338_200_DN
source_species_code: MM
GEO_id: GSE24574
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in BCL6 [GeneID=604] high follicular helper T cells versus naïve T CD4 [GeneID=920] cells.

description_full:
[cell repeats an earlier one in this file: 182 characters]


systematic_name: M8336
exact_source: GSE24574_2340_200_UP
source_species_code: MM
GEO_id: GSE24574
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in BCL6 [GeneID=604] low follicular helper T cells versus naïve CD4 [GeneID=620] T cells.

description_full:
[cell repeats an earlier one in this file: 182 characters]


systematic_name: M8339
exact_source: GSE24574_2340_200_DN
source_species_code: MM
GEO_id: GSE24574
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in BCL6 [GeneID=604] low follicular helper T cells versus naïve CD4 [GeneID=620] T cells.

description_full:
[cell repeats an earlier one in this file: 182 characters]


systematic_name: M8346
exact_source: GSE28449_2448_200_DN
source_species_code: MM
GEO_id: GSE28449
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in germinal center B lymphocytes: wildtype versus ZBTB7A [GeneID=51341] knockout.

description_full:
  B cells are indispensable for humoral immunity, as they ultimately give rise to antibody-secreting plasma cells. During T cell-dependent antibody responses, naive B cells form germinal centers (GCs), a distinct histologic structure found in secondary lymphoid organs. Naive B cells become activated upon interaction with T cells and antigen presenting cells, and begin to rapidly proliferate and form the characteristic GC structure. To elucidate the overall effect of LRF loss in the GCB cell transcriptome, gene expression microarray analysis of FACS-sorted GCB cells was performed. LRF Flox/+ mb-1 Cre+ mice were used as a control to normalize the potential effects of Cre recombinase, and four RNA samples for each genotype were used for the analysis.


systematic_name: M8347
exact_source: GSE28449_2448_200_UP
source_species_code: MM
GEO_id: GSE28449
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in germinal center B lymphocytes: wildtype versus ZBTB7A [GeneID=51341] knockout.

description_full:
  B cells are indispensable for humoral immunity, as they ultimately give rise to antibody-secreting plasma cells. During T cell-dependent antibody responses, naive B cells form germinal centers (GCs), a distinct histologic structure found in secondary lymphoid organs. Naive B cells become activated upon interaction with T cells and antigen presenting cells, and begin to rapidly proliferate and form the characteristic GC structure. To elucidate the overall effect of LRF loss in the GCB cell transcriptome, gene expression microarray analysis of FACS-sorted GCB cells was performed. LRF Flox/+ mb-1 Cre+ mice were used as a control to normalize the potential effects of Cre recombinase, and four RNA samples for each genotype were used for the analysis.


description_brief: Genes up-regulated in atherosclerosis macrophages: anti miR-33 versus untreated.
systematic_name: M8351
exact_source: GSE28783_3378_200_UP
source_species_code: MM
GEO_id: GSE28783
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  Inhibition of miR-33 results in increased cholesterol efflux and HDL-cholesterol levels in mice. In this study we examined the effect of miR-33 inhibition in a mouse model of atherosclerosis and observed significant reduction in atherosclerotic plaque size. At the end of the study, gene expression in macrophages from the atherosclerotic plaques was assessed. The results demonstrated a reduction in inflammatory gene expression and increased levels of mRNAs containing miR-33 binding sites.


description_brief: Genes down-regulated in T reg: natural versus induced cells.
systematic_name: M8359
exact_source: GSE19512_2400_200_DN
source_species_code: MM
GEO_id: GSE19512
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  The relative contribution of induced and natural Foxp3+ regulatory T cells (iTreg and nTreg cells, respectively) to the maintenance of tolerance is unknown. We examined their respective roles by in vivo adoptive transfer immunotherapy of newborn Foxp3-deficient BALB/c mice. Survival, weight gain, tissue infiltration, T cell activation, and the concentration of proinflammatory cytokines were used as outcome measurements. Treatment with iTreg cells alone was not successful. While effective in preventing death, treatment with nTreg cells alone was associated with chronic inflammation and autoimmunity. Outcomes markedly improved when conventional T (Tconv) cells were transferred together with the nTreg cells, where 10% of the peripheral Treg cell pool was derived by in-situ conversion. This enhancement depended upon the capacity of Tconv cells to express Foxp3. The gene expression profile of in vivo derived iTreg cells was similar to the established nTreg cell genetic signature. These results identify iTreg cells as an essential regulatory subset that supplements tolerance maintained by nTreg cells.


description_brief: Genes down-regulated in T reg from: peripheral blood versus cord blood.
systematic_name: M8367
exact_source: GSE22501_3835_200_DN
source_species_code: HS
GEO_id: GSE22501
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  Since the role of cord blood (CB) regulatory T cells (Tregs) for the suppression of the allogeneic T-cell response is under investigation, we analyzed and compared the functional properties and gene expression profile of Tregs expanded from CB units or from the peripheral blood (PB) of helathy donors. Tregs were purified from 23 CB units and from the PB of 13 donors and expanded for 6 days with anti-CD3, anti-CD28 and IL-2. Immunophenotypic analyses were performed, and suppressor activity of expanded Tregs was measured in mixed lymphocyte reaction (MLR) cultures. The IL-10 production capacity was tested and gene expression profile experiments were performed on 6 Tregs from PB and 4 from CB. CB and PB Tregs had similar immunophenotypic features. Tregs from CB presented a higher expansion capacity and genomic characterization showed in CB-derived Tregs a significant enrichments of genes involved in cell proliferation, chromatin modification and regulation of gene expression in CB-derived Tregs. All samples were positive for the Foxp3 gene and protein after expansion. CB and PB expanded Tregs exerted a comparable and potent suppressive function of MLR and presented a high in vitro IL-10 production capacity. Gene profile analysis also revealed for PB Tregs a significant enrichments of genes involved in the adaptive immune response.


description_brief: Genes up-regulated in CD4 [GeneID=920] T cells: untreated versus TGFB1 [GeneID=7040].
systematic_name: M8371
exact_source: GSE22025_3459_200_UP
source_species_code: HS
GEO_id: GSE22025
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  We examined the global gene expression pattern of T cells regulated by progesterone to gain further insights into the regulatory mechanisms of progesterone. We found 325-347 cord blood T cell genes up or down-regulated by P4 in the presence or absence of exogenous TGFb1. Peripheral blood T cells were relatively unresponsive with only 30-70 genes regulated by P4. IL-6 receptor (IL-6R) expression was greatly down-regulated by progesterone in cord blood, but not PB, T cells. Overall, these differences in gene expression are consistent with the differential responses of cord blood and peripheral blood T cells to progesterone. To gain insights into the differences of progesterone and control dendritic cells, we performed a microarray study and found ~180 genes regulated by progesterone in dendritic cells. The gene expression information suggests that progesterone has the potential to alter dendritic cell responses to cytokines, chemokine production, and migration which in combination would control T cell differentiation.


systematic_name: M8379
exact_source: GSE22025_3461_200_DN
source_species_code: HS
GEO_id: GSE22025
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T cells: progesterone [PubChem=5994] versus TGFB1 [GeneID=7040] and progesterone [PubChem=5994].

description_full:
  We examined the global gene expression pattern of T cells regulated by progesterone to gain further insights into the regulatory mechanisms of progesterone. We found 325-347 cord blood T cell genes up or down-regulated by P4 in the presence or absence of exogenous TGFb1. Peripheral blood T cells were relatively unresponsive with only 30-70 genes regulated by P4. IL-6 receptor (IL-6R) expression was greatly down-regulated by progesterone in cord blood, but not PB, T cells. Overall, these differences in gene expression are consistent with the differential responses of cord blood and peripheral blood T cells to progesterone. To gain insights into the differences of progesterone and control dendritic cells, we performed a microarray study and found ~180 genes regulated by progesterone in dendritic cells. The gene expression information suggests that progesterone has the potential to alter dendritic cell responses to cytokines, chemokine production, and migration which in combination would control T cell differentiation.


systematic_name: M8380
exact_source: GSE22025_3462_200_UP
source_species_code: HS
GEO_id: GSE22025
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T cells: TGFB1 [GeneID=7040] versus TGFB1 [GeneID=7040] and progesterone [PubChem=5994].

description_full:
[cell repeats an earlier one in this file: 1031 characters]


systematic_name: M8381
exact_source: GSE22025_3461_200_UP
source_species_code: HS
GEO_id: GSE22025
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T cells: progesterone [PubChem=5994] versus TGFB1 [GeneID=7040] and progesterone [PubChem=5994].

description_full:
[cell repeats an earlier one in this file: 1031 characters]


systematic_name: M8383
exact_source: GSE22025_3460_200_UP
source_species_code: HS
GEO_id: GSE22025
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T cells: untreated versus TGFB1 [GeneID=7040] and progesterone [PubChem=5994].

description_full:
[cell repeats an earlier one in this file: 1031 characters]


systematic_name: M8386
exact_source: GSE22025_3460_200_DN
source_species_code: HS
GEO_id: GSE22025
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T cells: untreated versus TGFB1 [GeneID=7040] and progesterone [PubChem=5994].

description_full:
[cell repeats an earlier one in this file: 1031 characters]


systematic_name: M8388
exact_source: GSE22025_3462_200_DN
source_species_code: HS
GEO_id: GSE22025
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T cells: TGFB1 [GeneID=7040] versus TGFB1 [GeneID=7040] and progesterone [PubChem=5994].

description_full:
[cell repeats an earlier one in this file: 1031 characters]


description_brief: Genes down-regulated in brain microglia versus bone marrow monocytes.
systematic_name: M8389
exact_source: GSE29949_3447_200_DN
source_species_code: MM
GEO_id: GSE29949
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  To understand the functional relationship between brain dendritic cells (brain DCs) and other myeloid cells, we compared the gene expression profile of m/chDCs to that of bone marrow monocytes, brain microglia and classical spleen CD8+ and CD8- DCs. In order to obtain enough brain DCs for mRNA extraction, we expanded brain DCs with in vivo Flt3L treatment before purification.


description_brief: Genes down-regulated in lin- cells: TCF7 [GeneID=6932] knockout versus wildtype.
systematic_name: M8422
exact_source: GSE26559_2842_200_DN
source_species_code: MM
GEO_id: GSE26559
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  Tcf1 is necessary for optimal T lineage development. Tcf1 deficient progenitors fail to initiate the T lineage program in vitro and development is severely defective in vivo. We used microarrays to assess the overal global gene expression differences from Tcf1 wildtype and deficient lymphoid biased progenitors cultures on Notch-ligand expressing stroma to determine if Tcf1 deficient progenitors are able to intiate the T lineage specification program. Abstract of manuscript: The thymus imposes the T cell fate on incoming multipotent progenitors, but the molecular mechanisms are poorly understood. We show that transcription factor Tcf1 initiates T-lineage-specific gene expression. Tcf1 is downstream of Notch1 signaling and expressed in early T-cell progenitors. Progenitors deficient for Tcf1 are unable to initiate normal T-lineage specification. Conversely, ectopic expression of Tcf1 in hematopoietic progenitors is sufficient to induce expression of T-lineage specific genes in vitro. Thus, our study identifies Tcf1 as critically involved in the establishment T cell identity.


description_brief: Genes down-regulated in B lymphocytes: systemic lupus erythematosous (SLE) versus healthy.
systematic_name: M8424
exact_source: GSE30153_3539_200_DN
source_species_code: HS
GEO_id: GSE30153
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  Systemic lupus erythematosous (SLE) is an autoimmune disease with an important clinical and biological heterogeneity. B lymphocytes appear central to the development of SLE which is characterized by the production of a large variety of autoantibodies and hypergammaglobulinemia. In mice, immature B cells from spontaneous lupus prone animals are able to produce autoantibodies when transferred into immunodeficient mice, strongly suggesting the existence of intrinsic B cell defects during lupus. In order to approach these defects in humans, we compared the peripheral B cell transcriptomes of quiescent lupus patients to normal B cell transcriptomes.


description_brief: Genes up-regulated in pre-B cells: STAT5 knockout versus wildtype.
systematic_name: M8426
exact_source: GSE24814_3047_200_UP
source_species_code: MM
GEO_id: GSE24814
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  In order to investigate the function of STAT5 in ALL, we isolated bone marrow cells from STAT5 fl/fl mice and transformed them with BCR-ABL1. In a second transduction the BCR-ABL1 driven pre-B cells were transformed either with CRE-GFP or empty vector control (GFP) and subjected to gene expression analysis.


description_brief: Genes up-regulated in CD8 T cells: effector memory versus naïve.
systematic_name: M8428
exact_source: GSE23321_2650_200_UP
source_species_code: HS
GEO_id: GSE23321
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  An early-differentiated CD8+ memory T cell subset with stem cell-like properties (TSCM) can be identified within the naïve-like T cell population by the expression of CD95/Fas. Based on experiments including exon- and gene-level expression analysis, we provide evidence that this subset of antigen-specific cells represents an early precursor of conventional central (TCM) and effector (TEM) memory CD8+ T cells with enhanced self-renewal capacity and proliferative potential. We identified 900 genes differentially expressed between major T cell subsets defined along with memory T cell commitment. Based on the analysis of these genes, CD95+ naïve T cells (TSCM) cluster closer to the CD8+ T memory compartment than to classical (CD95-) naïve T (TN) cells, and display an intermittent phenotype between classical TN and TCM cells in terms of all major T cell differentiation markers analyzed.


description_brief: Genes up-regulated in lung innate lymphoid cells versus spleen CD4 [GeneID=920] T cells.
systematic_name: M8443
exact_source: GSE46468_3662_200_UP
source_species_code: MM
GEO_id: GSE46468
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  Innate lymphoid cells (ILCs) are a recently recognized heterogenous group of immune cells that are critical in orchestrating immunity and inflammation in the intestine, but whether ILCs influence immune responses or tissue homeostasis at other mucosal sites remains poorly characterized. Here we identify a population of lung-resident ILCs in mice and humans that expressed the alloantigen Thy-1 (CD90), interleukin 2 (IL-2) receptor a-chain (CD25), IL-7 receptor a-chain (CD127) and the IL-33 receptor subunit T1-ST2. Notably, mouse ILCs accumulated in the lung after infection with influenza virus, and depletion of ILCs resulted in loss of airway epithelial integrity, diminished lung function and impaired airway remodeling. These defects were restored by administration of the lung ILC product amphiregulin. Collectively, our results demonstrate a critical role for lung ILCs in restoring airway epithelial integrity and tissue homeostasis after infection with influenza virus. As part of this study, we performed gene expression profiling to examine how the transcriptional signatures compared between murine naïve group 2 lung ILC and group 3 splenic LTi cell populations.


systematic_name: M8446
exact_source: GSE27291_3197_200_UP
source_species_code: HS
GEO_id: GSE27291
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in gamma delta T cells activated by phophoantigen BrHPP and IL2 [GeneID=3558]: 0h versus 6h.

description_full:
  We used microarrays to detail the global programme of gene expression by circulating TCRVgamma9+ gamma delta T cells isolated from healthy individuals,tested either as resting cells or cells activated by phosphoantigen BrHPP and IL-2at an early(+6hrs) and a late (+7days) timepoint. We find that with more “NK cell” genes than alphabeta T cells and more “T cell” genes than NK cells, the circulating TCRVgamma9+ gamma delta T cells cells have a hybrid transcriptome. The gene signature of the activated cells recapitulates their physiological functions: Th1 cytokine, chemokine and cytotoxic activities at first and mitotic activity at later time points. The gene expression pattern of activated normal gamma delta T cells is nevertheless clearly distinctive from that of NK/T and peripheral T cell lymphomas of the gamma delta subtype.


systematic_name: M8452
exact_source: GSE27291_3198_200_UP
source_species_code: HS
GEO_id: GSE27291
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in gamma delta T cells activated by phophoantigen BrHPP and IL2 [GeneID=3558]: 0h versus 7 days.

description_full:
  We used microarrays to detail the global programme of gene expression by circulating TCRVgamma9+ gamma delta T cells isolated from healthy individuals,tested either as resting cells or cells activated by phosphoantigen BrHPP and IL-2at an early(+6hrs) and a late (+7days) timepoint. We find that with more “NK cell” genes than alphabeta T cells and more “T cell” genes than NK cells, the circulating TCRVgamma9+ gamma delta T cells cells have a hybrid transcriptome. The gene signature of the activated cells recapitulates their physiological functions: Th1 cytokine, chemokine and cytotoxic activities at first and mitotic activity at later time points. The gene expression pattern of activated normal gamma delta T cells is nevertheless clearly distinctive from that of NK/T and peripheral T cell lymphomas of the gamma delta subtype.


systematic_name: M8453
exact_source: GSE27291_3197_200_DN
source_species_code: HS
GEO_id: GSE27291
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in gamma delta T cells activated by phophoantigen BrHPP and IL2 [GeneID=3558]: 0h versus 6h.

description_full:
  We used microarrays to detail the global programme of gene expression by circulating TCRVgamma9+ gamma delta T cells isolated from healthy individuals,tested either as resting cells or cells activated by phosphoantigen BrHPP and IL-2at an early(+6hrs) and a late (+7days) timepoint. We find that with more “NK cell” genes than alphabeta T cells and more “T cell” genes than NK cells, the circulating TCRVgamma9+ gamma delta T cells cells have a hybrid transcriptome. The gene signature of the activated cells recapitulates their physiological functions: Th1 cytokine, chemokine and cytotoxic activities at first and mitotic activity at later time points. The gene expression pattern of activated normal gamma delta T cells is nevertheless clearly distinctive from that of NK/T and peripheral T cell lymphomas of the gamma delta subtype.


systematic_name: M8457
exact_source: GSE27291_3198_200_DN
source_species_code: HS
GEO_id: GSE27291
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in gamma delta T cells activated by phophoantigen BrHPP and IL2 [GeneID=3558]: 0h versus 7 days.

description_full:
[cell repeats an earlier one in this file: 836 characters]


systematic_name: M8459
exact_source: GSE27291_3199_200_UP
source_species_code: HS
GEO_id: GSE27291
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in gamma delta T cells activated by phosphoantigen BrHPP and IL2 [GeneID=3558]: 6h versus 7 days.

description_full:
[cell repeats an earlier one in this file: 836 characters]


systematic_name: M8460
exact_source: GSE27291_3199_200_DN
source_species_code: HS
GEO_id: GSE27291
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in gamma delta T cells activated by phosphoantigen BrHPP and IL2 [GeneID=3558]: 6h versus 7 days.

description_full:
[cell repeats an earlier one in this file: 836 characters]


systematic_name: M8462
exact_source: GSE32533_3154_200_UP
source_species_code: MM
GEO_id: GSE32533
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in activated CD4 [GeneID=920] T cells: wildtype versus over-expressing MIR17 [GeneID=406952].

description_full:
  miR-17 from the miR-17-92 cluster regulate activation-induced cell death in T cells and modulate inducible regulatory T cell differentiation. We used microarrays to detail the global program of gene expression modulated by miR-17 and aim to identify the potential targets of miR-17.


systematic_name: M8464
exact_source: GSE32533_3153_200_DN
source_species_code: MM
GEO_id: GSE32533
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in activated CD4 [GeneID=920] T cells: wildtype versus MIR17 [GeneID=406952] knockout.

description_full:
  miR-17 from the miR-17-92 cluster regulate activation-induced cell death in T cells and modulate inducible regulatory T cell differentiation. We used microarrays to detail the global program of gene expression modulated by miR-17 and aim to identify the potential targets of miR-17.


systematic_name: M8465
exact_source: GSE32533_3154_200_DN
source_species_code: MM
GEO_id: GSE32533
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in activated CD4 [GeneID=920] T cells: wildtype versus over-expressing MIR17 [GeneID=406952].

description_full:
  miR-17 from the miR-17-92 cluster regulate activation-induced cell death in T cells and modulate inducible regulatory T cell differentiation. We used microarrays to detail the global program of gene expression modulated by miR-17 and aim to identify the potential targets of miR-17.


systematic_name: M8468
exact_source: GSE32533_3155_200_UP
source_species_code: MM
GEO_id: GSE32533
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in activated CD4 [GeneID=920] T cells with MIR17 [GeneID=406952] perturbation: knockout versus over-expression.

description_full:
[cell repeats an earlier one in this file: 282 characters]


systematic_name: M8469
exact_source: GSE32533_3153_200_UP
source_species_code: MM
GEO_id: GSE32533
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in activated CD4 [GeneID=920] T cells: wildtype versus MIR17 [GeneID=406952] knockout.

description_full:
[cell repeats an earlier one in this file: 282 characters]


systematic_name: M8470
exact_source: GSE32533_3155_200_DN
source_species_code: MM
GEO_id: GSE32533
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in activated CD4 [GeneID=920] T cells with MIR17 [GeneID=406952] perturbation: knockout versus over-expression.

description_full:
[cell repeats an earlier one in this file: 282 characters]


description_brief: Genes down-regulated in splenic B lymphocytes: wildtype versus KLF3 [GeneID=51274] knockout.
systematic_name: M8471
exact_source: GSE31622_2717_200_DN
source_species_code: MM
GEO_id: GSE31622
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  To investigate the roles of Klf3 in B lymphopoiesis, CD19+ B cells were sorted from the spleens of WT and Klf3 KO mice (Molecular and Cellular Biology (2008); 28:3967–3978). Following RNA extraction, gene expression was compared in WT and Klf3 KO CD19+splenic B cells using Affymetrix microarrays.


systematic_name: M8476
exact_source: GSE26351_2245_200_DN
source_species_code: HS
GEO_id: GSE26351
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD34+ [GeneID=947] cells: control versus treated with GSK-3 Inhibitor IX (BIO) [PubChem=5287844].

description_full:
  Analysis of mobilized peripheral blood CD34+ cells from a healthy volunteer under erythroid differentiation conditions with and without stimulation to the BMP or Wnt signaling pathways. For erythroid differentiation, expanded CD34+ cells were placed in Stemspan SFEM medium supplemented with 2% pen/strep, 20ng/ml SCF, 1U/ml Epo, 5ng/ml IL3, 2uM dexamethasone, and 1uM beta-estradiol. Arrays were performed 2 hours after addition of cytokines. For signaling pathway stimulation, cells were exposed to 0.5uM BIO (a GSK3 inhibitor) for Wnt pathway activation, 25ng/ml rhBMP4 for BMP pathway activation, or vehicle control for 2 hours. Three biological replicates were performed per treatment group. We used microarrays to detail the global program of gene expression changes after Wnt or BMP pathway stimulation in human CD34+ hematopoietic progenitors under erythroid differentiation conditions.


systematic_name: M8477
exact_source: GSE26351_2247_200_UP
source_species_code: HS
GEO_id: GSE26351
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD34+ [GeneID=947] cells treated with GSK-3 Inhibitor IX (BIO) [PubChem=5287844] versus those stimulated by BMP4 [GeneID=652].

description_full:
  Analysis of mobilized peripheral blood CD34+ cells from a healthy volunteer under erythroid differentiation conditions with and without stimulation to the BMP or Wnt signaling pathways. For erythroid differentiation, expanded CD34+ cells were placed in Stemspan SFEM medium supplemented with 2% pen/strep, 20ng/ml SCF, 1U/ml Epo, 5ng/ml IL3, 2uM dexamethasone, and 1uM beta-estradiol. Arrays were performed 2 hours after addition of cytokines. For signaling pathway stimulation, cells were exposed to 0.5uM BIO (a GSK3 inhibitor) for Wnt pathway activation, 25ng/ml rhBMP4 for BMP pathway activation, or vehicle control for 2 hours. Three biological replicates were performed per treatment group. We used microarrays to detail the global program of gene expression changes after Wnt or BMP pathway stimulation in human CD34+ hematopoietic progenitors under erythroid differentiation conditions.


systematic_name: M8480
exact_source: GSE26351_2247_200_DN
source_species_code: HS
GEO_id: GSE26351
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD34+ [GeneID=947] cells treated with GSK-3 Inhibitor IX (BIO) [PubChem=5287844] versus those stimulated by BMP4 [GeneID=652].

description_full:
  Analysis of mobilized peripheral blood CD34+ cells from a healthy volunteer under erythroid differentiation conditions with and without stimulation to the BMP or Wnt signaling pathways. For erythroid differentiation, expanded CD34+ cells were placed in Stemspan SFEM medium supplemented with 2% pen/strep, 20ng/ml SCF, 1U/ml Epo, 5ng/ml IL3, 2uM dexamethasone, and 1uM beta-estradiol. Arrays were performed 2 hours after addition of cytokines. For signaling pathway stimulation, cells were exposed to 0.5uM BIO (a GSK3 inhibitor) for Wnt pathway activation, 25ng/ml rhBMP4 for BMP pathway activation, or vehicle control for 2 hours. Three biological replicates were performed per treatment group. We used microarrays to detail the global program of gene expression changes after Wnt or BMP pathway stimulation in human CD34+ hematopoietic progenitors under erythroid differentiation conditions.


systematic_name: M8482
exact_source: GSE26351_2245_200_UP
source_species_code: HS
GEO_id: GSE26351
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD34+ [GeneID=947] cells: control versus treated with GSK-3 Inhibitor IX (BIO) [PubChem=5287844].

description_full:
[cell repeats an earlier one in this file: 894 characters]


systematic_name: M8484
exact_source: GSE29164_2437_200_UP
source_species_code: MM
GEO_id: GSE29164
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in B16 melanoma (day 3): untreated versus mock treatment during adoptive transfer therapy.

description_full:
  Myeloid-derived cells comprising the tumor stroma represent a heterogeneous population of cells critical to the structure, function and growth of established cancers. We have recently found that engineering tumor-specific CD8+ T cells to secrete IL-12 (IL-12TD) can lead to striking improvements in T-cell activity against established melanomas in murine models. Surprisingly, IL-12-dependent enhancement of CD8+ T-cell anti-tumor function did not occur through direct ligation of receptors on lymphocytes or NK cells. Instead, IL-12 sensitized host bone marrow-derived tumor-stromal cells, partly through interferon-gamma, to indirectly enhance the effects of adoptively-transferred T cells. Direct presentation of antigen by tumor was not necessary, but MHC class I expression on endogenous cells was essential for IL-12 mediated anti-tumor enhancements. Upon successful treatment with IL-12TD cells, we observed the selective elimination of tumor-infiltrating CD11b+ F4/80+ macrophages, CD11b+/ClassII+/CD11c+ dendritic cells and CD11b+/Ly6C+/Ly6G- but not CD11b+/Ly6C+/Ly6G+ myeloid-derived suppressor cells within regressing lesions. These results are consistent with a model whereby IL-12 triggers the maturation of myeloid-derived cells into competent antigen cross-presenting cells. Licensed recognition of these antigens by effector T cells may in turn trigger the collapse of the tumor stroma and aid in the regression of large vascularized lesions.


systematic_name: M8485
exact_source: GSE29164_2437_200_DN
source_species_code: MM
GEO_id: GSE29164
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in B16 melanoma (day 3): untreated versus mock treatment during adoptive transfer therapy.

description_full:
  Myeloid-derived cells comprising the tumor stroma represent a heterogeneous population of cells critical to the structure, function and growth of established cancers. We have recently found that engineering tumor-specific CD8+ T cells to secrete IL-12 (IL-12TD) can lead to striking improvements in T-cell activity against established melanomas in murine models. Surprisingly, IL-12-dependent enhancement of CD8+ T-cell anti-tumor function did not occur through direct ligation of receptors on lymphocytes or NK cells. Instead, IL-12 sensitized host bone marrow-derived tumor-stromal cells, partly through interferon-gamma, to indirectly enhance the effects of adoptively-transferred T cells. Direct presentation of antigen by tumor was not necessary, but MHC class I expression on endogenous cells was essential for IL-12 mediated anti-tumor enhancements. Upon successful treatment with IL-12TD cells, we observed the selective elimination of tumor-infiltrating CD11b+ F4/80+ macrophages, CD11b+/ClassII+/CD11c+ dendritic cells and CD11b+/Ly6C+/Ly6G- but not CD11b+/Ly6C+/Ly6G+ myeloid-derived suppressor cells within regressing lesions. These results are consistent with a model whereby IL-12 triggers the maturation of myeloid-derived cells into competent antigen cross-presenting cells. Licensed recognition of these antigens by effector T cells may in turn trigger the collapse of the tumor stroma and aid in the regression of large vascularized lesions.


systematic_name: M8488
exact_source: GSE29164_2443_200_UP
source_species_code: MM
GEO_id: GSE29164
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in mock treatment during adoptive transfer therapy of B16 melanoma: day 3 versus day 7.

description_full:
[cell repeats an earlier one in this file: 1459 characters]


systematic_name: M8494
exact_source: GSE29164_2443_200_DN
source_species_code: MM
GEO_id: GSE29164
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in mock treatment during adoptive transfer therapy of B16 melanoma: day 3 versus day 7.

description_full:
[cell repeats an earlier one in this file: 1459 characters]


systematic_name: M8497
exact_source: GSE29164_2440_200_UP
source_species_code: MM
GEO_id: GSE29164
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in B16 melanoma (day 7): untreated versus mock treatment during adoptive transfer therapy.

description_full:
[cell repeats an earlier one in this file: 1459 characters]


systematic_name: M8498
exact_source: GSE29164_2440_200_DN
source_species_code: MM
GEO_id: GSE29164
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in B16 melanoma (day 7): untreated versus mock treatment during adoptive transfer therapy.

description_full:
[cell repeats an earlier one in this file: 1459 characters]


systematic_name: M8506
exact_source: GSE23568_2920_200_DN
source_species_code: MM
GEO_id: GSE23568
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD8 T cells: over-expressing ID3 [GeneID=3399] versus ID3 [GeneID=3399] knockout.

description_full:
  Mouse CD8+ T cells affected by ID3 (Inhibitor of DNA binding 3) display patterns of gene expression suggesting enhanced persistance and survival. In this study, we identified genes differentially expressed between ID32a transduced and mock transduced, and ID32a knockout and wild type mouse CD8+ T cells. Most prominent functions of differentially expressed genes include DNA replication-associated repair, maintenance of chromosome stability and mitotic cell divison machinery. Overall, these data suggest that ID3 acts in favor of maintained survival in CD8+ mouse T cells.


systematic_name: M8517
exact_source: GSE23568_2920_200_UP
source_species_code: MM
GEO_id: GSE23568
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD8 T cells: over-expressing ID3 [GeneID=3399] versus ID3 [GeneID=3399] knockout.

description_full:
[cell repeats an earlier one in this file: 575 characters]


description_brief: Genes down-regulated in macrophages: resting differentiated versus alternatively activated M2.
systematic_name: M8524
exact_source: GSE32164_3500_200_DN
source_species_code: HS
GEO_id: GSE32164
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  In response to microenvironmental signals macrophages undergo different activation, indicated as classic/M1 and alternative/M2 polarization. C-Myc transcription factor could be an essential player in M2 polarization. Functional relevance of c-Myc in M2 macrophage biology is investigated by evaluating the effect of 100-58F4, on the transcriptional profile induced on human macrophages by IL-4.


systematic_name: M8533
exact_source: GSE33374_3499_200_DN
source_species_code: HS
GEO_id: GSE33374
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in KLRB1 high [GeneID=3820] T cells: CD8A [GeneID=925] versus CD8A CD8B [GeneID=925;926].

description_full:
  We used microarrays to compare gene expression between healthy human CD161++CD8aa and CD161++CD8ab T cells.


description_brief: Genes up-regulated in CD8 T cells: KLRB1 high [GeneID=3820] versus KLRB1 int [GeneID=3820].
systematic_name: M8534
exact_source: GSE33424_3490_200_UP
source_species_code: HS
GEO_id: GSE33424
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  We used microarray to compare gene expression between CD161++/CD161+/CD161-CD8+ T cells from human cord blood.


systematic_name: M8538
exact_source: GSE33374_3499_200_UP
source_species_code: HS
GEO_id: GSE33374
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in KLRB1 high [GeneID=3820] T cells: CD8A [GeneID=925] versus CD8A CD8B [GeneID=925;926].

description_full:
  We used microarrays to compare gene expression between healthy human CD161++CD8aa and CD161++CD8ab T cells.


description_brief: Genes down-regulated in effector CD8 T cells: CXCR1+ [GeneID=3577] versus CXCR1- [GeneID=3577].
systematic_name: M8558
exact_source: GSE26890_3493_200_DN
source_species_code: HS
GEO_id: GSE26890
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  Effector CD8+ T cells are believed to be terminally differentiated cells having cytotoxic activity and the ability to produce effector cytokines such as INF-γ and TNF-α. We investigated the difference between CXCR1+ and CXCR1- subsets of human effector CD27-CD28-CD8+ T cells. Both subsets similarly expressed cytolytic molecules and exerted substantial cytolytic activity, whereas only the CXCR1- subset had IL-2 productivity and self-proliferative activity and was more resistant to cell death than the CXCR1+ subset. These differences were explained by the specific up-regulation of CAMK4, SPRY2, and IL-7R in the CXCR1- subset and that of pro-apoptotic DAPK1 in the CXCR1+ subset. The IL-2 producers were more frequently found in the IL-7R+ subset of the CXCR1- effector CD8+ T cells than in the IL-7R- subset. IL-7/IL-7R signaling promoted cell survival only in the CXCR1- subset. The present study has highlighted a novel subset of effector CD8+ T cells producing IL-2 and suggests the importance of this subset in the homeostasis of effector CD8+ T cells.


description_brief: Genes down-regulated in T helper cells 5 days post polarization: Th1 versus Th17.
systematic_name: M8561
exact_source: GSE26030_2562_200_DN
source_species_code: MM
GEO_id: GSE26030
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  Serial comparison between Th1 and Th17 tumor-specific cells cultured in vitro and ex vivo after transferred into sublethaly irradiated B6.PL mice. Th17-derived cells acquire Th1-like properties in vivo but maintain a distinct molecular profile.


systematic_name: M8567
exact_source: GSE26030_2568_200_UP
source_species_code: MM
GEO_id: GSE26030
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in Th1 cells 5 days post polarization: control versus stimulated with anti-CD3 and anti-CD28.

description_full:
[cell repeats an earlier one in this file: 244 characters]


systematic_name: M8568
exact_source: GSE26030_2568_200_DN
source_species_code: MM
GEO_id: GSE26030
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in Th1 cells 5 days post polarization: control versus stimulated with anti-CD3 and anti-CD28.

description_full:
[cell repeats an earlier one in this file: 244 characters]


systematic_name: M8569
exact_source: GSE26030_2569_200_UP
source_species_code: MM
GEO_id: GSE26030
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in Th1 cells 15 days post polarization: control versus stimulated with anti-CD3 and anti-CD28.

description_full:
[cell repeats an earlier one in this file: 244 characters]


systematic_name: M8571
exact_source: GSE26030_2567_200_DN
source_species_code: MM
GEO_id: GSE26030
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in T helper cells 15 days post polarization and stimulated with anti-CD3 and anti-CD28: Th1 versus Th17.

description_full:
[cell repeats an earlier one in this file: 244 characters]


systematic_name: M8572
exact_source: GSE26030_2565_200_DN
source_species_code: MM
GEO_id: GSE26030
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in Th17 cells 15 days post polarization: control versus stimulated with anti-CD3 and anti-CD28.

description_full:
[cell repeats an earlier one in this file: 244 characters]


systematic_name: M8573
exact_source: GSE26030_2566_200_UP
source_species_code: MM
GEO_id: GSE26030
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in T helper cells 5 days post polarization and stimulated with anti-CD3 and anti-CD28: Th1 versus Th17.

description_full:
[cell repeats an earlier one in this file: 244 characters]


systematic_name: M8574
exact_source: GSE26030_2566_200_DN
source_species_code: MM
GEO_id: GSE26030
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in T helper cells 5 days post polarization and stimulated with anti-CD3 and anti-CD28: Th1 versus Th17.

description_full:
[cell repeats an earlier one in this file: 244 characters]


systematic_name: M8576
exact_source: GSE26030_2569_200_DN
source_species_code: MM
GEO_id: GSE26030
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in Th1 cells 15 days post polarization: control versus stimulated with anti-CD3 and anti-CD28.

description_full:
[cell repeats an earlier one in this file: 244 characters]


systematic_name: M8578
exact_source: GSE26030_2565_200_UP
source_species_code: MM
GEO_id: GSE26030
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in Th17 cells 15 days post polarization: control versus stimulated with anti-CD3 and anti-CD28.

description_full:
[cell repeats an earlier one in this file: 244 characters]


systematic_name: M8579
exact_source: GSE26030_2564_200_UP
source_species_code: MM
GEO_id: GSE26030
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in Th17 cells 5 days post polarization: control versus stimulated with anti-CD3 and anti-CD28.

description_full:
[cell repeats an earlier one in this file: 244 characters]


systematic_name: M8580
exact_source: GSE26030_2567_200_UP
source_species_code: MM
GEO_id: GSE26030
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in T helper cells 15 days post polarization and stimulated with anti-CD3 and anti-CD28: Th1 versus Th17.

description_full:
[cell repeats an earlier one in this file: 244 characters]


systematic_name: M8581
exact_source: GSE26030_2564_200_DN
source_species_code: MM
GEO_id: GSE26030
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in Th17 cells 5 days post polarization: control versus stimulated with anti-CD3 and anti-CD28.

description_full:
[cell repeats an earlier one in this file: 244 characters]


systematic_name: M8584
exact_source: GSE22313_3102_200_DN
source_species_code: MM
GEO_id: GSE22313
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T cells: healthy versus systemic lupus erythematosus (SLE).

description_full:
  Sle1a.1 is part of the Sle1a lupus susceptibility locus which results in the production of activated and autoreactive CD4+ T cells as well as a reduction in the peripheral regulatory T cell (Treg) pool. Sle1a.1 CD4+ T cells showed a defective response to retinoic acid (RA) expansion of TGFβ-induced Tregs. At the molecular level, Sle1a.1 corresponds to an increased expression of a novel splice isoform of Pbx1, Pbx1-d. Pbx1-d over-expression is sufficient to induce an activated/inflammatory phenotype in Jurkat T cells, and to decrease their apoptotic response to RA. PBX1-d is expressed more frequently in lupus patients than in healthy controls, and its presence correlates with an increased memory T cell population. These findings indicate that Pbx1 is a novel lupus susceptibility gene that regulates T cell activation and tolerance.


systematic_name: M8587
exact_source: GSE27859_2497_200_DN
source_species_code: MM
GEO_id: GSE27859
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in macrophages versus dendritic cells sorted as ITGAX int [GeneID=3687] and EMR1 int [GeneID=2015].

description_full:
  Dendritic cells (DCs) and macrophages (MPs) are important for immunological homeostasis in the colon. We found that F4/80hi CX3CR1hi (CD11b+CD103-) cells account for 80% of mouse colonic lamina propria (cLP) MHC-IIhi cells. Both CD11c+ and CD11c- cells within this population were identified as MPs based on multiple criteria, including a MP transcriptome revealed by microarray analysis. These MPs constitutively released high levels of IL-10 at least partially in response to the microbiota via an MyD88-independent mechanism. In contrast, cells expressing low to intermediate levels of F4/80 and CX3CR1 were identified as DCs, based on phenotypic and functional analysis and comprise three separate CD11chi cell populations: CD103+CX3CR1-CD11b- DCs, CD103+CX3CR1-CD11b+ DCs and CD103-CX3CR1intCD11b+ DCs. In non-inflammatory conditions, Ly6Chi monocytes differentiated primarily into CD11c+, but not CD11c- MPs. In contrast, during colitis, Ly6Chi monocytes massively invaded the colon and differentiated into pro-inflammatory CD103-CX3CR1intCD11b+ DCs, which produced high levels of IL-12, IL-23, iNOS and TNF. These findings demonstrate the dual capacity of Ly6Chi blood monocytes to differentiate into either regulatory MPs or inflammatory DCs in the colon, and that the balance of these immunologically antagonistic cell types is dictated by microenvironmental conditions.


systematic_name: M8589
exact_source: GSE27859_2496_200_DN
source_species_code: MM
GEO_id: GSE27859
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in macrophages versus those sorted as ITGAX int [GeneID=3687] and EMR1 high [GeneID=2015].

description_full:
  Dendritic cells (DCs) and macrophages (MPs) are important for immunological homeostasis in the colon. We found that F4/80hi CX3CR1hi (CD11b+CD103-) cells account for 80% of mouse colonic lamina propria (cLP) MHC-IIhi cells. Both CD11c+ and CD11c- cells within this population were identified as MPs based on multiple criteria, including a MP transcriptome revealed by microarray analysis. These MPs constitutively released high levels of IL-10 at least partially in response to the microbiota via an MyD88-independent mechanism. In contrast, cells expressing low to intermediate levels of F4/80 and CX3CR1 were identified as DCs, based on phenotypic and functional analysis and comprise three separate CD11chi cell populations: CD103+CX3CR1-CD11b- DCs, CD103+CX3CR1-CD11b+ DCs and CD103-CX3CR1intCD11b+ DCs. In non-inflammatory conditions, Ly6Chi monocytes differentiated primarily into CD11c+, but not CD11c- MPs. In contrast, during colitis, Ly6Chi monocytes massively invaded the colon and differentiated into pro-inflammatory CD103-CX3CR1intCD11b+ DCs, which produced high levels of IL-12, IL-23, iNOS and TNF. These findings demonstrate the dual capacity of Ly6Chi blood monocytes to differentiate into either regulatory MPs or inflammatory DCs in the colon, and that the balance of these immunologically antagonistic cell types is dictated by microenvironmental conditions.


systematic_name: M8591
exact_source: GSE27859_2500_200_UP
source_species_code: MM
GEO_id: GSE27859
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in cells sorted as ITGAX int [GeneID=3687]: EMR1 high [GeneID=2015] macrophages versus EMR1 int [GeneID=2015] dendritic cells.

description_full:
[cell repeats an earlier one in this file: 1379 characters]


systematic_name: M8593
exact_source: GSE27859_2496_200_UP
source_species_code: MM
GEO_id: GSE27859
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in macrophages versus those sorted as ITGAX int [GeneID=3687] and EMR1 high [GeneID=2015].

description_full:
[cell repeats an earlier one in this file: 1379 characters]


systematic_name: M8594
exact_source: GSE27859_2497_200_UP
source_species_code: MM
GEO_id: GSE27859
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in macrophages versus dendritic cells sorted as ITGAX int [GeneID=3687] and EMR1 int [GeneID=2015].

description_full:
[cell repeats an earlier one in this file: 1379 characters]


systematic_name: M8595
exact_source: GSE27859_2498_200_DN
source_species_code: MM
GEO_id: GSE27859
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in dendritic cells versus macrophages sorted as ITGAX int [GeneID=3687] and EMR1 high [GeneID=2015].

description_full:
[cell repeats an earlier one in this file: 1379 characters]


systematic_name: M8596
exact_source: GSE27859_2499_200_UP
source_species_code: MM
GEO_id: GSE27859
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in dendritic cells versus those sorted as ITGAX int [GeneID=3687] and EMR1 int [GeneID=2015].

description_full:
[cell repeats an earlier one in this file: 1379 characters]


systematic_name: M8597
exact_source: GSE27859_2498_200_UP
source_species_code: MM
GEO_id: GSE27859
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in dendritic cells versus macrophages sorted as ITGAX int [GeneID=3687] and EMR1 high [GeneID=2015].

description_full:
[cell repeats an earlier one in this file: 1379 characters]


systematic_name: M8598
exact_source: GSE27859_2500_200_DN
source_species_code: MM
GEO_id: GSE27859
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in cells sorted as ITGAX int [GeneID=3687]: EMR1 high [GeneID=2015] macrophages versus EMR1 int [GeneID=2015] dendritic cells.

description_full:
[cell repeats an earlier one in this file: 1379 characters]


systematic_name: M8600
exact_source: GSE27859_2499_200_DN
source_species_code: MM
GEO_id: GSE27859
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in dendritic cells versus those sorted as ITGAX int [GeneID=3687] and EMR1 int [GeneID=2015].

description_full:
[cell repeats an earlier one in this file: 1379 characters]


systematic_name: M8602
exact_source: GSE32128_2969_200_DN
source_species_code: MM
GEO_id: GSE32128
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in T cell activation mechanism that was NOS2 [GeneID=4843] dependent versus NOS2 [GeneID=4843] independent activation.

description_full:
  Comparison of two Chlamydia-specific CD4 T cells that are dependent on iNOS to terminate Chlamydia replication in epithelial cells to two Chlamydia-specific CD4 T cells that are iNOS-independent: Chlamydia trachomatis urogenital serovars replicate predominately in epithelial cells lining the reproductive tract. This tissue tropism poses a unique challenge for the host immune system and vaccine development. Studies utilizing the Chlamydia muridarum mouse model have shown that CD4 T cells are critical and sufficient to clear primary genital tract infections. In vitro studies have shown that CD4 T cells terminate the infection in epithelial cells by up regulating epithelial iNOS transcription and nitric oxide production via IFN-gamma and T cell-epithelial cell interactions mediated by LFA-1-ICAM-1. This mechanism however is not critical as iNOS-deficient mice clear infections normally, and IFN-gamma deficient mice clear 99.9% of the infection with near normal kinetics. We recently showed that a subset of Chlamydia-specific CD4 T cell clones were able to terminate replication in epithelial cells using a mechanism that was independent of iNOS and IFN-gamma. That mechanism did not require physical lysis of infected cells, but instead required T cell degranulation. In this study we advanced that work using gene expression microarrays to compare CD4 T cell clones that are able to terminate epithelial replication via an iNOS-independent mechanism to iNOS-dependent CD4 T cell clones. Micro array experiments showed that Plac8 was differentially expressed by the T cell clones having the iNOS-independent mechanism. Plac8-deficient mice had significantly delayed clearance of C. muridarum genital tract infections, and that the large majority of Plac8-deficient mice treated with the iNOS-inhibitor N-monomethyl-L-arginine (MLA) were unable to resolve a C. muridarum genital tract infection over 8 weeks. These results demonstrate that there are two independent and redundant T cell mechanisms for clearing C. muridarum genital tract infections; one mechanism dependent on iNOS, the other mechanism dependent on Plac8. While T cells subsets have been defined by cytokine profiles, there are important subdivisions by effector functions, in this case CD4Plac8.


systematic_name: M8605
exact_source: GSE32128_2969_200_UP
source_species_code: MM
GEO_id: GSE32128
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in T cell activation mechanism that was NOS2 [GeneID=4843] dependent versus NOS2 [GeneID=4843] independent activation.

description_full:
  Comparison of two Chlamydia-specific CD4 T cells that are dependent on iNOS to terminate Chlamydia replication in epithelial cells to two Chlamydia-specific CD4 T cells that are iNOS-independent: Chlamydia trachomatis urogenital serovars replicate predominately in epithelial cells lining the reproductive tract. This tissue tropism poses a unique challenge for the host immune system and vaccine development. Studies utilizing the Chlamydia muridarum mouse model have shown that CD4 T cells are critical and sufficient to clear primary genital tract infections. In vitro studies have shown that CD4 T cells terminate the infection in epithelial cells by up regulating epithelial iNOS transcription and nitric oxide production via IFN-gamma and T cell-epithelial cell interactions mediated by LFA-1-ICAM-1. This mechanism however is not critical as iNOS-deficient mice clear infections normally, and IFN-gamma deficient mice clear 99.9% of the infection with near normal kinetics. We recently showed that a subset of Chlamydia-specific CD4 T cell clones were able to terminate replication in epithelial cells using a mechanism that was independent of iNOS and IFN-gamma. That mechanism did not require physical lysis of infected cells, but instead required T cell degranulation. In this study we advanced that work using gene expression microarrays to compare CD4 T cell clones that are able to terminate epithelial replication via an iNOS-independent mechanism to iNOS-dependent CD4 T cell clones. Micro array experiments showed that Plac8 was differentially expressed by the T cell clones having the iNOS-independent mechanism. Plac8-deficient mice had significantly delayed clearance of C. muridarum genital tract infections, and that the large majority of Plac8-deficient mice treated with the iNOS-inhibitor N-monomethyl-L-arginine (MLA) were unable to resolve a C. muridarum genital tract infection over 8 weeks. These results demonstrate that there are two independent and redundant T cell mechanisms for clearing C. muridarum genital tract infections; one mechanism dependent on iNOS, the other mechanism dependent on Plac8. While T cells subsets have been defined by cytokine profiles, there are important subdivisions by effector functions, in this case CD4Plac8.


systematic_name: M8606
exact_source: GSE32986_3110_200_DN
source_species_code: MM
GEO_id: GSE32986
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in bone marrow-derived dendritic cells: unstimulated versus CSF2 [GeneID=1437] and high dose of 1,3-beta-D-oligoglucan [PubChem=11375554].

description_full:
  A simultaneous engagement of different pathogen recognition receptors provides a tailor made adaptive immunity for an efficient defence against distinct pathogens. For example, cross talk of TLR and c-type lectin signalling effectively shapes distinct gene expression patterns by integrating the signals at the level of NF-κB. Here, we extend this principle to a strong synergism between the Dectin-1 agonist, curdlan, and an inflammatory growth factor, GM-CSF. Both together act in synergy in inducing a strong inflammatory signature which converts immature DCs to potent effector DCs. A variety of cytokines (IL-1β, IL-6, TNF-α, IL-2 and IL-12p70), costimulatory molecules (CD80, CD86, CD40 and CD70), chemokines (CxCl1, CxCl2, CxCl3, CCl12, CCl17) as well as receptors and molecules involved in fugal recognition and immunity such as Mincle, Dectin-1, Dectin-2 and Pentraxin 3 are strongly up-regulated in DC treated simultaneously with curdlan and GM-CSF. The synergistic effect of both stimuli resulted in strong IKBα phosphorylation, in its rapid degradation and in enhanced nuclear translocation of all NF-κB subunits. We further identified MAPK ERK, as one possible integration site of both signals, since its phosphorylation was clearly augmented when curdlan was co-applied with GM-CSF. Our data demonstrate that the immunomodulatory activity of curdlan requires an additional signal provided by GM-CSF to successfully initiate a robust β-glucan specific cytokine and chemokine response. The integration of both signals clearly prime and tailor a more effective innate and adaptive response against invading microbes and fungi.


systematic_name: M8608
exact_source: GSE32986_3110_200_UP
source_species_code: MM
GEO_id: GSE32986
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in bone marrow-derived dendritic cells: unstimulated versus CSF2 [GeneID=1437] and high dose of 1,3-beta-D-oligoglucan [PubChem=11375554].

description_full:
  A simultaneous engagement of different pathogen recognition receptors provides a tailor made adaptive immunity for an efficient defence against distinct pathogens. For example, cross talk of TLR and c-type lectin signalling effectively shapes distinct gene expression patterns by integrating the signals at the level of NF-κB. Here, we extend this principle to a strong synergism between the Dectin-1 agonist, curdlan, and an inflammatory growth factor, GM-CSF. Both together act in synergy in inducing a strong inflammatory signature which converts immature DCs to potent effector DCs. A variety of cytokines (IL-1β, IL-6, TNF-α, IL-2 and IL-12p70), costimulatory molecules (CD80, CD86, CD40 and CD70), chemokines (CxCl1, CxCl2, CxCl3, CCl12, CCl17) as well as receptors and molecules involved in fugal recognition and immunity such as Mincle, Dectin-1, Dectin-2 and Pentraxin 3 are strongly up-regulated in DC treated simultaneously with curdlan and GM-CSF. The synergistic effect of both stimuli resulted in strong IKBα phosphorylation, in its rapid degradation and in enhanced nuclear translocation of all NF-κB subunits. We further identified MAPK ERK, as one possible integration site of both signals, since its phosphorylation was clearly augmented when curdlan was co-applied with GM-CSF. Our data demonstrate that the immunomodulatory activity of curdlan requires an additional signal provided by GM-CSF to successfully initiate a robust β-glucan specific cytokine and chemokine response. The integration of both signals clearly prime and tailor a more effective innate and adaptive response against invading microbes and fungi.


systematic_name: M8610
exact_source: GSE32986_3111_200_UP
source_species_code: MM
GEO_id: GSE32986
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in bone marrow-derived dendritic cells CSF2 [GeneID=1437] versus CSF2 [GeneID=1437] and low dose of 1,3-beta-D-oligoglucan [PubChem=11375554].

description_full:
[cell repeats an earlier one in this file: 1637 characters]


systematic_name: M8611
exact_source: GSE32986_3111_200_DN
source_species_code: MM
GEO_id: GSE32986
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in bone marrow-derived dendritic cells CSF2 [GeneID=1437] versus CSF2 [GeneID=1437] and low dose of 1,3-beta-D-oligoglucan [PubChem=11375554].

description_full:
[cell repeats an earlier one in this file: 1637 characters]


systematic_name: M8612
exact_source: GSE32986_3107_200_DN
source_species_code: MM
GEO_id: GSE32986
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in bone marrow-derived dendritic cells: unstimulated versus low dose of 1,3-beta-D-oligoglucan [PubChem=11375554].

description_full:
[cell repeats an earlier one in this file: 1637 characters]


systematic_name: M8614
exact_source: GSE32986_3108_200_UP
source_species_code: MM
GEO_id: GSE32986
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in bone marrow-derived dendritic cells: unstimulated versus high dose of 1,3-beta-D-oligoglucan [PubChem=11375554].

description_full:
[cell repeats an earlier one in this file: 1637 characters]


systematic_name: M8618
exact_source: GSE32986_3108_200_DN
source_species_code: MM
GEO_id: GSE32986
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in bone marrow-derived dendritic cells: unstimulated versus high dose of 1,3-beta-D-oligoglucan [PubChem=11375554].

description_full:
[cell repeats an earlier one in this file: 1637 characters]


systematic_name: M8619
exact_source: GSE32986_3109_200_UP
source_species_code: MM
GEO_id: GSE32986
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in bone marrow-derived dendritic cells: unstimulated versus CSF2 [GeneID=1437] and low dose of 1,3-beta-D-oligoglucan [PubChem=11375554].

description_full:
[cell repeats an earlier one in this file: 1637 characters]


systematic_name: M8620
exact_source: GSE32986_3109_200_DN
source_species_code: MM
GEO_id: GSE32986
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in bone marrow-derived dendritic cells: unstimulated versus CSF2 [GeneID=1437] and low dose of 1,3-beta-D-oligoglucan [PubChem=11375554].

description_full:
[cell repeats an earlier one in this file: 1637 characters]


systematic_name: M8622
exact_source: GSE32986_3116_200_DN
source_species_code: MM
GEO_id: GSE32986
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in bone marrow-derived dendritic cells treated by CSF2 [GeneID=1437] and 1,3-beta-D-oligoglucan [PubChem=11375554]: low dose versus high dose.

description_full:
[cell repeats an earlier one in this file: 1637 characters]


systematic_name: M8624
exact_source: GSE32986_3112_200_DN
source_species_code: MM
GEO_id: GSE32986
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in bone marrow-derived dendritic cells CSF2 [GeneID=1437] versus CSF2 [GeneID=1437] and high dose of 1,3-beta-D-oligoglucan [PubChem=11375554].

description_full:
[cell repeats an earlier one in this file: 1637 characters]


systematic_name: M8625
exact_source: GSE32986_3113_200_UP
source_species_code: MM
GEO_id: GSE32986
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in bone marrow-derived dendritic cells: low dose of 1,3-beta-D-oligoglucan [PubChem=11375554] versus CSF2 [GeneID=1437] and low dose of 1,3-beta-D-oligoglucan [PubChem=11375554].

description_full:
[cell repeats an earlier one in this file: 1637 characters]


systematic_name: M8628
exact_source: GSE32986_3113_200_DN
source_species_code: MM
GEO_id: GSE32986
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in bone marrow-derived dendritic cells: low dose of 1,3-beta-D-oligoglucan [PubChem=11375554] versus CSF2 [GeneID=1437] and low dose of 1,3-beta-D-oligoglucan [PubChem=11375554].

description_full:
[cell repeats an earlier one in this file: 1637 characters]


systematic_name: M8630
exact_source: GSE32986_3112_200_UP
source_species_code: MM
GEO_id: GSE32986
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in bone marrow-derived dendritic cells CSF2 [GeneID=1437] versus CSF2 [GeneID=1437] and high dose of 1,3-beta-D-oligoglucan [PubChem=11375554].

description_full:
[cell repeats an earlier one in this file: 1637 characters]


systematic_name: M8631
exact_source: GSE32986_3114_200_DN
source_species_code: MM
GEO_id: GSE32986
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in bone marrow-derived dendritic cells: high dose of 1,3-beta-D-oligoglucan [PubChem=11375554] versus CSF2 [GeneID=1437] and high dose of 1,3-beta-D-oligoglucan [PubChem=11375554].

description_full:
[cell repeats an earlier one in this file: 1637 characters]


systematic_name: M8632
exact_source: GSE32986_3115_200_UP
source_species_code: MM
GEO_id: GSE32986
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in bone marrow-derived dendritic cells treated with 1,3-beta-D-oligoglucan [PubChem=11375554]: low dose versus high dose.

description_full:
[cell repeats an earlier one in this file: 1637 characters]


systematic_name: M8635
exact_source: GSE32986_3115_200_DN
source_species_code: MM
GEO_id: GSE32986
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in bone marrow-derived dendritic cells treated with 1,3-beta-D-oligoglucan [PubChem=11375554]: low dose versus high dose.

description_full:
[cell repeats an earlier one in this file: 1637 characters]


systematic_name: M8636
exact_source: GSE32986_3114_200_UP
source_species_code: MM
GEO_id: GSE32986
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in bone marrow-derived dendritic cells: high dose of 1,3-beta-D-oligoglucan [PubChem=11375554] versus CSF2 [GeneID=1437] and high dose of 1,3-beta-D-oligoglucan [PubChem=11375554].

description_full:
[cell repeats an earlier one in this file: 1637 characters]


systematic_name: M8638
exact_source: GSE32986_3107_200_UP
source_species_code: MM
GEO_id: GSE32986
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in bone marrow-derived dendritic cells: unstimulated versus low dose of 1,3-beta-D-oligoglucan [PubChem=11375554].

description_full:
[cell repeats an earlier one in this file: 1637 characters]


systematic_name: M8639
exact_source: GSE32986_3116_200_UP
source_species_code: MM
GEO_id: GSE32986
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in bone marrow-derived dendritic cells treated by CSF2 [GeneID=1437] and 1,3-beta-D-oligoglucan [PubChem=11375554]: low dose versus high dose.

description_full:
[cell repeats an earlier one in this file: 1637 characters]


systematic_name: M8641
exact_source: GSE32986_3106_200_DN
source_species_code: MM
GEO_id: GSE32986
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in bone marrow-derived dendritic cells: unstimulated versus CSF2 [GeneID=1437].

description_full:
[cell repeats an earlier one in this file: 1637 characters]


description_full: Gene expression from WT and NFAT5 KO primary macrophage cultures.
systematic_name: M8642
exact_source: GSE26343_2486_200_UP
source_species_code: MM
GEO_id: GSE26343
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in bone marrow-derived macrophages stimulated with LPS: wildtype versus NFAT5 [GeneID=10725] knockout.


description_full: Gene expression from WT and NFAT5 KO primary macrophage cultures.
systematic_name: M8643
exact_source: GSE26343_2484_200_DN
source_species_code: MM
GEO_id: GSE26343
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in bone marrow-derived macrophages with NFAT5 [GeneID=10725] knockout: control versus stimulated with LPS.


description_full: Gene expression from WT and NFAT5 KO primary macrophage cultures.
systematic_name: M8644
exact_source: GSE26343_2485_200_UP
source_species_code: MM
GEO_id: GSE26343
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in bone marrow-derived macrophages: wildtype versus NFAT5 [GeneID=10725] knockout.


description_full: Gene expression from WT and NFAT5 KO primary macrophage cultures.
systematic_name: M8647
exact_source: GSE26343_2485_200_DN
source_species_code: MM
GEO_id: GSE26343
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in bone marrow-derived macrophages: wildtype versus NFAT5 [GeneID=10725] knockout.


description_full: Gene expression from WT and NFAT5 KO primary macrophage cultures.
systematic_name: M8649
exact_source: GSE26343_2484_200_UP
source_species_code: MM
GEO_id: GSE26343
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in bone marrow-derived macrophages with NFAT5 [GeneID=10725] knockout: control versus stimulated with LPS.


description_full: Gene expression from WT and NFAT5 KO primary macrophage cultures.
systematic_name: M8651
exact_source: GSE26343_2486_200_DN
source_species_code: MM
GEO_id: GSE26343
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in bone marrow-derived macrophages stimulated with LPS: wildtype versus NFAT5 [GeneID=10725] knockout.


description_brief: Genes up-regulated in P14 CD8+ T cells: ST2 [GeneID=6761] knockout versus wildtype.
systematic_name: M8653
exact_source: GSE34392_2699_200_UP
source_species_code: MM
GEO_id: GSE34392
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  Pathogen-associated molecular patterns decisively influence antiviral immune responses, whereas the contribution of endogenous signals of tissue damage, also known as “damage-associated molecular patterns” or “alarmins”, remains ill-defined. We show that interleukin-33 (IL-33), an alarmin released from necrotic cells, is necessary for potent CD8+ T cell (CTL) responses to replicating, prototypic RNA and DNA viruses in mice. IL-33 signaled through its receptor on activated CTLs, enhanced clonal expansion in a MyD88-dependent, CTL-intrinsic fashion, determined polyfunctional effector cell differentiation and was necessary for virus control. Moreover, recombinant IL-33 augmented vaccine-induced CTL responses. Radio-resistant cells of the splenic T cell zone produced IL-33, and efficient CTL responses required IL-33 from radio-resistant cells but not from hematopoietic cells. Thus, alarmin release by radio-resistant cells orchestrates protective antiviral CTL responses.


systematic_name: M8656
exact_source: GSE35825_3221_200_DN
source_species_code: MM
GEO_id: GSE35825
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in bone marrow-derived macrophages: interferon alpha versus IFNG [GeneID=3458].

description_full:
  We used microarrays to compare interferon-alpha (IFNa)- and interferon-gamma (IFNg)-stimulated genes under an equivalent biological input. The goal was to compare IFNa- and IFNg-stimulated genes, as well as to identify common and distinct sets of type I and II ISGs.


systematic_name: M8657
exact_source: GSE35825_3220_200_UP
source_species_code: MM
GEO_id: GSE35825
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in bone marrow-derived macrophages: untreated versus stimulated by IFNG [GeneID=3458].

description_full:
  We used microarrays to compare interferon-alpha (IFNa)- and interferon-gamma (IFNg)-stimulated genes under an equivalent biological input. The goal was to compare IFNa- and IFNg-stimulated genes, as well as to identify common and distinct sets of type I and II ISGs.


systematic_name: M8658
exact_source: GSE35825_3219_200_UP
source_species_code: MM
GEO_id: GSE35825
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in bone marrow-derived macrophages: untreated versus stimulated by interferon alpha.

description_full:
  We used microarrays to compare interferon-alpha (IFNa)- and interferon-gamma (IFNg)-stimulated genes under an equivalent biological input. The goal was to compare IFNa- and IFNg-stimulated genes, as well as to identify common and distinct sets of type I and II ISGs.


systematic_name: M8661
exact_source: GSE35825_3219_200_DN
source_species_code: MM
GEO_id: GSE35825
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in bone marrow-derived macrophages: untreated versus stimulated by interferon alpha.

description_full:
[cell repeats an earlier one in this file: 266 characters]


systematic_name: M8662
exact_source: GSE35825_3220_200_DN
source_species_code: MM
GEO_id: GSE35825
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in bone marrow-derived macrophages: untreated versus stimulated by IFNG [GeneID=3458].

description_full:
[cell repeats an earlier one in this file: 266 characters]


systematic_name: M8664
exact_source: GSE34156_2942_200_DN
source_species_code: HS
GEO_id: GSE34156
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in monocytes (6h): untreated versus muramyl dipeptide [PubChem=11620162] andM. tuberculosis 19 kDa lipopeptide.

description_full:
  human blood monocytes were isolated, activated and harvested at several timepoints In this study, we identified genes that were differentially expressed in human monocytes activated with eiter NOD2L and/or TLR2/1L.


systematic_name: M8668
exact_source: GSE34156_2942_200_UP
source_species_code: HS
GEO_id: GSE34156
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in monocytes (6h): untreated versus muramyl dipeptide [PubChem=11620162] andM. tuberculosis 19 kDa lipopeptide.

description_full:
[cell repeats an earlier one in this file: 214 characters]


systematic_name: M8670
exact_source: GSE34156_2948_200_DN
source_species_code: HS
GEO_id: GSE34156
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in monocytes (24h): untreated versus muramyl dipeptide [PubChem=11620162] andM. tuberculosis 19 kDa lipopeptide.

description_full:
[cell repeats an earlier one in this file: 214 characters]


systematic_name: M8671
exact_source: GSE34156_2949_200_UP
source_species_code: HS
GEO_id: GSE34156
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in monocytes (24h): muramyl dipeptide [PubChem=11620162] versus M. tuberculosis 19 kDa lipopeptide.

description_full:
[cell repeats an earlier one in this file: 214 characters]


systematic_name: M8674
exact_source: GSE34156_2948_200_UP
source_species_code: HS
GEO_id: GSE34156
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in monocytes (24h): untreated versus muramyl dipeptide [PubChem=11620162] andM. tuberculosis 19 kDa lipopeptide.

description_full:
[cell repeats an earlier one in this file: 214 characters]


systematic_name: M8675
exact_source: GSE34156_2950_200_DN
source_species_code: HS
GEO_id: GSE34156
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in monocytes (24h): muramyl dipeptide [PubChem=11620162] versus muramyl dipeptide [PubChem=11620162] and M. tuberculosis 19 kDa lipopeptide.

description_full:
[cell repeats an earlier one in this file: 214 characters]


systematic_name: M8676
exact_source: GSE34156_2951_200_UP
source_species_code: HS
GEO_id: GSE34156
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in monocytes (24h): M. tuberculosis 19 kDa lipopeptide versus M. tuberculosis 19 kDa lipopeptide and muramyl dipeptide [PubChem=11620162].

description_full:
[cell repeats an earlier one in this file: 214 characters]


systematic_name: M8678
exact_source: GSE34156_2949_200_DN
source_species_code: HS
GEO_id: GSE34156
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in monocytes (24h): muramyl dipeptide [PubChem=11620162] versus M. tuberculosis 19 kDa lipopeptide.

description_full:
[cell repeats an earlier one in this file: 214 characters]


systematic_name: M8679
exact_source: GSE34156_2950_200_UP
source_species_code: HS
GEO_id: GSE34156
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in monocytes (24h): muramyl dipeptide [PubChem=11620162] versus muramyl dipeptide [PubChem=11620162] and M. tuberculosis 19 kDa lipopeptide.

description_full:
[cell repeats an earlier one in this file: 214 characters]


systematic_name: M8680
exact_source: GSE34156_2945_200_DN
source_species_code: HS
GEO_id: GSE34156
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in monocytes (6h): M. tuberculosis 19 kDa lipopeptide versus M. tuberculosis 19 kDa lipopeptide and muramyl dipeptide [PubChem=11620162].

description_full:
[cell repeats an earlier one in this file: 214 characters]


systematic_name: M8686
exact_source: GSE34156_2943_200_DN
source_species_code: HS
GEO_id: GSE34156
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in monocytes (6h): muramyl dipeptide [PubChem=11620162] versus M. tuberculosis 19 kDa lipopeptide.

description_full:
[cell repeats an earlier one in this file: 214 characters]


systematic_name: M8687
exact_source: GSE34156_2944_200_UP
source_species_code: HS
GEO_id: GSE34156
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in monocytes (6h): muramyl dipeptide [PubChem=11620162] versus muramyl dipeptide [PubChem=11620162] and M. tuberculosis 19 kDa lipopeptide.

description_full:
[cell repeats an earlier one in this file: 214 characters]


systematic_name: M8688
exact_source: GSE34156_2944_200_DN
source_species_code: HS
GEO_id: GSE34156
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in monocytes (6h): muramyl dipeptide [PubChem=11620162] versus muramyl dipeptide [PubChem=11620162] and M. tuberculosis 19 kDa lipopeptide.

description_full:
[cell repeats an earlier one in this file: 214 characters]


systematic_name: M8690
exact_source: GSE34156_2943_200_UP
source_species_code: HS
GEO_id: GSE34156
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in monocytes (6h): muramyl dipeptide [PubChem=11620162] versus M. tuberculosis 19 kDa lipopeptide.

description_full:
[cell repeats an earlier one in this file: 214 characters]


systematic_name: M8691
exact_source: GSE34156_2951_200_DN
source_species_code: HS
GEO_id: GSE34156
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in monocytes (24h): M. tuberculosis 19 kDa lipopeptide versus M. tuberculosis 19 kDa lipopeptide and muramyl dipeptide [PubChem=11620162].

description_full:
[cell repeats an earlier one in this file: 214 characters]


systematic_name: M8693
exact_source: GSE34156_2945_200_UP
source_species_code: HS
GEO_id: GSE34156
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in monocytes (6h): M. tuberculosis 19 kDa lipopeptide versus M. tuberculosis 19 kDa lipopeptide and muramyl dipeptide [PubChem=11620162].

description_full:
[cell repeats an earlier one in this file: 214 characters]


systematic_name: M8694
exact_source: GSE30971_2575_200_DN
source_species_code: MM
GEO_id: GSE30971
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in bone marrow-derived macrophages with MLL4 [GeneID=9757] knockout: 2h LPS versus 4h LPS.

description_full:
  Histone methyltransferases catalyze site-specific deposition of methyl groups, enabling recruitment of transcriptional regulators. In mammals, trimethylation of lysine 4 in histone H3, a modification localized at the transcription start sites of active genes, is catalyzed by six enzymes (SET1a and SET1b, MLL1–MLL4) whose specific functions are largely unknown. By using a genomic approach, we found that in macrophages, MLL4 (also known as Wbp7) was required for the expression of Pigp, an essential component of the GPI-GlcNAc transferase, the enzyme catalyzing the first step of glycosylphosphatidylinositol (GPI) anchor synthesis. Impaired Pigp expression in Wbp7-/- macrophages abolished GPI anchor-dependent loading of proteins on the cell membrane. Consistently, loss of GPI-anchored CD14, the coreceptor for lipopolysaccharide (LPS) and other bacterial molecules, markedly attenuated LPS-triggered intracellular signals and gene expression changes. These data link a histone-modifying enzyme to a biosynthetic pathway and indicate a specialized biological role for Wbp7 in macrophage function and antimicrobial response.


systematic_name: M8698
exact_source: GSE30971_2576_200_UP
source_species_code: MM
GEO_id: GSE30971
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in bone marrow-derived macrophages: heterozygous versus homozygous knockout of MLL4 [GeneID=9757].

description_full:
  Histone methyltransferases catalyze site-specific deposition of methyl groups, enabling recruitment of transcriptional regulators. In mammals, trimethylation of lysine 4 in histone H3, a modification localized at the transcription start sites of active genes, is catalyzed by six enzymes (SET1a and SET1b, MLL1–MLL4) whose specific functions are largely unknown. By using a genomic approach, we found that in macrophages, MLL4 (also known as Wbp7) was required for the expression of Pigp, an essential component of the GPI-GlcNAc transferase, the enzyme catalyzing the first step of glycosylphosphatidylinositol (GPI) anchor synthesis. Impaired Pigp expression in Wbp7-/- macrophages abolished GPI anchor-dependent loading of proteins on the cell membrane. Consistently, loss of GPI-anchored CD14, the coreceptor for lipopolysaccharide (LPS) and other bacterial molecules, markedly attenuated LPS-triggered intracellular signals and gene expression changes. These data link a histone-modifying enzyme to a biosynthetic pathway and indicate a specialized biological role for Wbp7 in macrophage function and antimicrobial response.


systematic_name: M8703
exact_source: GSE30971_2575_200_UP
source_species_code: MM
GEO_id: GSE30971
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in bone marrow-derived macrophages with MLL4 [GeneID=9757] knockout: 2h LPS versus 4h LPS.

description_full:
  Histone methyltransferases catalyze site-specific deposition of methyl groups, enabling recruitment of transcriptional regulators. In mammals, trimethylation of lysine 4 in histone H3, a modification localized at the transcription start sites of active genes, is catalyzed by six enzymes (SET1a and SET1b, MLL1–MLL4) whose specific functions are largely unknown. By using a genomic approach, we found that in macrophages, MLL4 (also known as Wbp7) was required for the expression of Pigp, an essential component of the GPI-GlcNAc transferase, the enzyme catalyzing the first step of glycosylphosphatidylinositol (GPI) anchor synthesis. Impaired Pigp expression in Wbp7-/- macrophages abolished GPI anchor-dependent loading of proteins on the cell membrane. Consistently, loss of GPI-anchored CD14, the coreceptor for lipopolysaccharide (LPS) and other bacterial molecules, markedly attenuated LPS-triggered intracellular signals and gene expression changes. These data link a histone-modifying enzyme to a biosynthetic pathway and indicate a specialized biological role for Wbp7 in macrophage function and antimicrobial response.


systematic_name: M8705
exact_source: GSE30971_2571_200_UP
source_species_code: MM
GEO_id: GSE30971
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in bone marrow-derived macrophages with heterozygous MLL4 [GeneID=9757] knockout: control versus treated with LPS for 4h.

description_full:
[cell repeats an earlier one in this file: 1129 characters]


systematic_name: M8707
exact_source: GSE30971_2571_200_DN
source_species_code: MM
GEO_id: GSE30971
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in bone marrow-derived macrophages with heterozygous MLL4 [GeneID=9757] knockout: control versus treated with LPS for 4h.

description_full:
[cell repeats an earlier one in this file: 1129 characters]


systematic_name: M8708
exact_source: GSE30971_2570_200_UP
source_species_code: MM
GEO_id: GSE30971
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in bone marrow-derived macrophages with heterozygous MLL4 [GeneID=9757] knockout: control versus treated with LPS for 2h.

description_full:
[cell repeats an earlier one in this file: 1129 characters]


systematic_name: M8709
exact_source: GSE30971_2570_200_DN
source_species_code: MM
GEO_id: GSE30971
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in bone marrow-derived macrophages with heterozygous MLL4 [GeneID=9757] knockout: control versus treated with LPS for 2h.

description_full:
[cell repeats an earlier one in this file: 1129 characters]


systematic_name: M8710
exact_source: GSE30971_2573_200_UP
source_species_code: MM
GEO_id: GSE30971
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in bone marrow-derived macrophages with MLL4 [GeneID=9757] knockout: control versus treated with LPS for 2h.

description_full:
[cell repeats an earlier one in this file: 1129 characters]


systematic_name: M8712
exact_source: GSE30971_2573_200_DN
source_species_code: MM
GEO_id: GSE30971
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in bone marrow-derived macrophages with MLL4 [GeneID=9757] knockout: control versus treated with LPS for 2h.

description_full:
[cell repeats an earlier one in this file: 1129 characters]


systematic_name: M8714
exact_source: GSE30971_2574_200_UP
source_species_code: MM
GEO_id: GSE30971
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in bone marrow-derived macrophages with MLL4 [GeneID=9757] knockout: control versus treated with LPS for 4h.

description_full:
[cell repeats an earlier one in this file: 1129 characters]


systematic_name: M8717
exact_source: GSE30971_2574_200_DN
source_species_code: MM
GEO_id: GSE30971
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in bone marrow-derived macrophages with MLL4 [GeneID=9757] knockout: control versus treated with LPS for 4h.

description_full:
[cell repeats an earlier one in this file: 1129 characters]


systematic_name: M8721
exact_source: GSE30971_2576_200_DN
source_species_code: MM
GEO_id: GSE30971
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in bone marrow-derived macrophages: heterozygous versus homozygous knockout of MLL4 [GeneID=9757].

description_full:
[cell repeats an earlier one in this file: 1129 characters]


systematic_name: M8722
exact_source: GSE30971_2577_200_UP
source_species_code: MM
GEO_id: GSE30971
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in bone marrow-derived macrophages treated with LPS for 2h: heterozygous versus homozygous knockout of MLL4 [GeneID=9757].

description_full:
[cell repeats an earlier one in this file: 1129 characters]


systematic_name: M8723
exact_source: GSE30971_2577_200_DN
source_species_code: MM
GEO_id: GSE30971
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in bone marrow-derived macrophages treated with LPS for 2h: heterozygous versus homozygous knockout of MLL4 [GeneID=9757].

description_full:
[cell repeats an earlier one in this file: 1129 characters]


systematic_name: M8724
exact_source: GSE30971_2572_200_UP
source_species_code: MM
GEO_id: GSE30971
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in bone marrow-derived macrophages with heterozygous MLL4 [GeneID=9757] knockout: 2h LPS versus 4h LPS.

description_full:
[cell repeats an earlier one in this file: 1129 characters]


systematic_name: M8725
exact_source: GSE30971_2572_200_DN
source_species_code: MM
GEO_id: GSE30971
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in bone marrow-derived macrophages with heterozygous MLL4 [GeneID=9757] knockout: 2h LPS versus 4h LPS.

description_full:
[cell repeats an earlier one in this file: 1129 characters]


systematic_name: M8726
exact_source: GSE30971_2578_200_DN
source_species_code: MM
GEO_id: GSE30971
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in bone marrow-derived macrophages treated with LPS for 4h: heterozygous versus homozygous knockout of MLL4 [GeneID=9757].

description_full:
[cell repeats an earlier one in this file: 1129 characters]


systematic_name: M8727
exact_source: GSE30971_2578_200_UP
source_species_code: MM
GEO_id: GSE30971
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in bone marrow-derived macrophages treated with LPS for 4h: heterozygous versus homozygous knockout of MLL4 [GeneID=9757].

description_full:
[cell repeats an earlier one in this file: 1129 characters]


systematic_name: M8730
exact_source: GSE36888_2361_200_UP
source_species_code: MM
GEO_id: GSE36888
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in T cells stimulated by IL2 [GeneID=3558] for 2h: STAT5 double knock-in versus wildtype.

description_full:
  Cytokine-activated STAT proteins dimerize and bind to high-affinity motifs, and N-terminal domain-mediated oligomerization of dimers allows tetramer formation and binding to low-affinity tandem motifs, but the functions of dimers versus tetramers are unknown. We generated Stat5a and Stat5b double knock-in (DKI) N-domain mutant mice that form dimers but not tetramers, identified cytokine-regulated genes whose expression required STAT5 tetramers, and defined consensus motifs for dimers versus tetramers. Whereas Stat5- deficient mice exhibited perinatal lethality, DKI mice were viable, indicating that STAT5 dimers were sufficient for survival. Nevertheless, STAT5 DKI mice had fewer CD4+CD25+ T cells, NK cells, and CD8+ T cells, with impaired cytokine-induced proliferation and homeostatic proliferation of CD8+ T cells. DKI CD8+ T cell proliferation following viral infection was diminished and DKI Treg cells did not efficiently control colitis. Thus, tetramerization of STAT5 is dispensable for survival but is critical for cytokine responses and normal immune function.


systematic_name: M8733
exact_source: GSE36888_2354_200_UP
source_species_code: MM
GEO_id: GSE36888
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in STAT5 double knock-in T cells: control versus IL2 [GeneID=3558] stimulation for 2h.

description_full:
  Cytokine-activated STAT proteins dimerize and bind to high-affinity motifs, and N-terminal domain-mediated oligomerization of dimers allows tetramer formation and binding to low-affinity tandem motifs, but the functions of dimers versus tetramers are unknown. We generated Stat5a and Stat5b double knock-in (DKI) N-domain mutant mice that form dimers but not tetramers, identified cytokine-regulated genes whose expression required STAT5 tetramers, and defined consensus motifs for dimers versus tetramers. Whereas Stat5- deficient mice exhibited perinatal lethality, DKI mice were viable, indicating that STAT5 dimers were sufficient for survival. Nevertheless, STAT5 DKI mice had fewer CD4+CD25+ T cells, NK cells, and CD8+ T cells, with impaired cytokine-induced proliferation and homeostatic proliferation of CD8+ T cells. DKI CD8+ T cell proliferation following viral infection was diminished and DKI Treg cells did not efficiently control colitis. Thus, tetramerization of STAT5 is dispensable for survival but is critical for cytokine responses and normal immune function.


systematic_name: M8737
exact_source: GSE36888_2356_200_UP
source_species_code: MM
GEO_id: GSE36888
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in STAT5 double knock-in T cells: control versus IL2 [GeneID=3558] stimulation for 6h.

description_full:
[cell repeats an earlier one in this file: 1079 characters]


systematic_name: M8738
exact_source: GSE36888_2356_200_DN
source_species_code: MM
GEO_id: GSE36888
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in STAT5 double knock-in T cells: control versus IL2 [GeneID=3558] stimulation for 6h.

description_full:
[cell repeats an earlier one in this file: 1079 characters]


systematic_name: M8742
exact_source: GSE36888_2358_200_UP
source_species_code: MM
GEO_id: GSE36888
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in STAT5 double knock-in T cells: control versus IL2 [GeneID=3558] stimulation for 17h.

description_full:
[cell repeats an earlier one in this file: 1079 characters]


systematic_name: M8743
exact_source: GSE36888_2358_200_DN
source_species_code: MM
GEO_id: GSE36888
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in STAT5 double knock-in T cells: control versus IL2 [GeneID=3558] stimulation for 17h.

description_full:
[cell repeats an earlier one in this file: 1079 characters]


systematic_name: M8744
exact_source: GSE36888_2362_200_UP
source_species_code: MM
GEO_id: GSE36888
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in T cells stimulated by IL2 [GeneID=3558] for 6h: STAT5 double knock-in versus wildtype.

description_full:
[cell repeats an earlier one in this file: 1079 characters]


systematic_name: M8745
exact_source: GSE36888_2362_200_DN
source_species_code: MM
GEO_id: GSE36888
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in T cells stimulated by IL2 [GeneID=3558] for 6h: STAT5 double knock-in versus wildtype.

description_full:
[cell repeats an earlier one in this file: 1079 characters]


systematic_name: M8748
exact_source: GSE36888_2363_200_UP
source_species_code: MM
GEO_id: GSE36888
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in T cells stimulated by IL2 [GeneID=3558] for 17h: STAT5 double knock-in versus wildtype.

description_full:
[cell repeats an earlier one in this file: 1079 characters]


systematic_name: M8750
exact_source: GSE36888_2361_200_DN
source_species_code: MM
GEO_id: GSE36888
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in T cells stimulated by IL2 [GeneID=3558] for 2h: STAT5 double knock-in versus wildtype.

description_full:
[cell repeats an earlier one in this file: 1079 characters]


systematic_name: M8755
exact_source: GSE36888_2363_200_DN
source_species_code: MM
GEO_id: GSE36888
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in T cells stimulated by IL2 [GeneID=3558] for 17h: STAT5 double knock-in versus wildtype.

description_full:
[cell repeats an earlier one in this file: 1079 characters]


systematic_name: M8757
exact_source: GSE36888_2354_200_DN
source_species_code: MM
GEO_id: GSE36888
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in STAT5 double knock-in T cells: control versus IL2 [GeneID=3558] stimulation for 2h.

description_full:
[cell repeats an earlier one in this file: 1079 characters]


description_brief: Genes up-regulated in CD16- monocytes versus dendritic cells.
systematic_name: M8761
exact_source: GSE34515_3421_200_UP
source_species_code: HS
GEO_id: GSE34515
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  In this study gene expression of human blood classical monocytes (CD14++CD16-), CD16 positive monocytes (consisting of non-classical CD14+16++ and intermediate CD14++CD16+ monocytes) and CD1c+ CD19- dendritic cells from healthy subjects were investigated.


description_brief: Genes up-regulated in dendritic cells with knockout of NLRP10 [GeneID=338322]: control versus LPS.
systematic_name: M8767
exact_source: GSE36009_2674_200_UP
source_species_code: MM
GEO_id: GSE36009
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  Nlrp10-deficient mice have a profound defect in helper T cell-driven immune responses. T cell priming is impaired due to a defect in the emigration of a dendritic cells from inflamed tissue and antigen transport to draining lymph nodes. DC chemotaxis to CCR7-dependent and independent ligands is intact in the absence of Nlrp10. Therefore to identify novel molecules potentially involved in Nlrp10-dependent DC function we used an unbiased gene array approach on Nlrp10-deficient BMDCs treated with or without LPS.


systematic_name: M8768
exact_source: GSE36009_2674_200_DN
source_species_code: MM
GEO_id: GSE36009
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in dendritic cells with knockout of NLRP10 [GeneID=338322]: control versus LPS.

description_full:
  Nlrp10-deficient mice have a profound defect in helper T cell-driven immune responses. T cell priming is impaired due to a defect in the emigration of a dendritic cells from inflamed tissue and antigen transport to draining lymph nodes. DC chemotaxis to CCR7-dependent and independent ligands is intact in the absence of Nlrp10. Therefore to identify novel molecules potentially involved in Nlrp10-dependent DC function we used an unbiased gene array approach on Nlrp10-deficient BMDCs treated with or without LPS.


systematic_name: M8769
exact_source: GSE36009_2673_200_UP
source_species_code: MM
GEO_id: GSE36009
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in dendritic cells in response to LPS: wildtype versus NLRP10 [GeneID=338322] knockout.

description_full:
  Nlrp10-deficient mice have a profound defect in helper T cell-driven immune responses. T cell priming is impaired due to a defect in the emigration of a dendritic cells from inflamed tissue and antigen transport to draining lymph nodes. DC chemotaxis to CCR7-dependent and independent ligands is intact in the absence of Nlrp10. Therefore to identify novel molecules potentially involved in Nlrp10-dependent DC function we used an unbiased gene array approach on Nlrp10-deficient BMDCs treated with or without LPS.


systematic_name: M8770
exact_source: GSE36009_2673_200_DN
source_species_code: MM
GEO_id: GSE36009
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in dendritic cells in response to LPS: wildtype versus NLRP10 [GeneID=338322] knockout.

description_full:
[cell repeats an earlier one in this file: 514 characters]


description_brief: Genes down-regulated in peritoneal macrophages: untreated versus poly(IC).
systematic_name: M8781
exact_source: GSE36891_2976_200_DN
source_species_code: MM
GEO_id: GSE36891
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  We have identified more than 50 genes that have upregulated expression in TLR3 activated (PMI-1,2), but have downregulated expression in TLR2 activated (PMP-1,2) macrophages, as compared to control cells (PMC-1,2)


systematic_name: M8784
exact_source: GSE36891_2978_200_DN
source_species_code: MM
GEO_id: GSE36891
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in peritoneal macrophages: poly(IC) versus Pam3Cys-Ser-(Lys)4 [PubChem=130704].

description_full:
  We have identified more than 50 genes that have upregulated expression in TLR3 activated (PMI-1,2), but have downregulated expression in TLR2 activated (PMP-1,2) macrophages, as compared to control cells (PMC-1,2)


systematic_name: M8790
exact_source: GSE37605_2581_200_DN
source_species_code: MM
GEO_id: GSE37605
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in T reg (FOXP3+ [GeneID=50943]) cells from B6 mice: Foxp3-Fusion-GFP versus Foxp3-ires-GFP.

description_full:
  The aim of this study was to quantify the impact of chimeric Foxp3-GFP protein on the Treg cell transcriptional program.


systematic_name: M8791
exact_source: GSE37605_2582_200_UP
source_species_code: MM
GEO_id: GSE37605
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in splenocytes from Foxp3-ires-GFP B6 mice: T reg (FOXP3+ [GeneID=50943]) versus T conv (FOXP3- [GeneID=50943]).

description_full:
  The aim of this study was to quantify the impact of chimeric Foxp3-GFP protein on the Treg cell transcriptional program.


systematic_name: M8792
exact_source: GSE37605_2581_200_UP
source_species_code: MM
GEO_id: GSE37605
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in T reg (FOXP3+ [GeneID=50943]) cells from B6 mice: Foxp3-Fusion-GFP versus Foxp3-ires-GFP.

description_full:
  The aim of this study was to quantify the impact of chimeric Foxp3-GFP protein on the Treg cell transcriptional program.


systematic_name: M8793
exact_source: GSE37605_2579_200_UP
source_species_code: MM
GEO_id: GSE37605
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in splenocytes from Foxp3-Fusion-GFP B6 mice: T reg (FOXP3+ [GeneID=50943]) versus T conv (FOXP3- [GeneID=50943]) cells.

description_full:
[cell repeats an earlier one in this file: 120 characters]


systematic_name: M8794
exact_source: GSE37605_2579_200_DN
source_species_code: MM
GEO_id: GSE37605
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in splenocytes from Foxp3-Fusion-GFP B6 mice: T reg (FOXP3+ [GeneID=50943]) versus T conv (FOXP3- [GeneID=50943]) cells.

description_full:
[cell repeats an earlier one in this file: 120 characters]


systematic_name: M8796
exact_source: GSE37605_2580_200_UP
source_species_code: MM
GEO_id: GSE37605
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in splenocytes from Foxp3-Fusion-GFP NOD mice: T reg (FOXP3+ [GeneID=50943]) versus T conv (FOXP3- [GeneID=50943]) cells.

description_full:
[cell repeats an earlier one in this file: 120 characters]


systematic_name: M8799
exact_source: GSE37605_2580_200_DN
source_species_code: MM
GEO_id: GSE37605
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in splenocytes from Foxp3-Fusion-GFP NOD mice: T reg (FOXP3+ [GeneID=50943]) versus T conv (FOXP3- [GeneID=50943]) cells.

description_full:
[cell repeats an earlier one in this file: 120 characters]


systematic_name: M8810
exact_source: GSE37605_2584_200_UP
source_species_code: MM
GEO_id: GSE37605
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in T reg (FOXP3+ [GeneID=50943]) cells from NOD mice: Foxp3-Fusion-GFP versus Foxp3-ires-GFP.

description_full:
[cell repeats an earlier one in this file: 120 characters]


systematic_name: M8811
exact_source: GSE37605_2582_200_DN
source_species_code: MM
GEO_id: GSE37605
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in splenocytes from Foxp3-ires-GFP B6 mice: T reg (FOXP3+ [GeneID=50943]) versus T conv (FOXP3- [GeneID=50943]).

description_full:
[cell repeats an earlier one in this file: 120 characters]


systematic_name: M8820
exact_source: GSE37605_2584_200_DN
source_species_code: MM
GEO_id: GSE37605
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in T reg (FOXP3+ [GeneID=50943]) cells from NOD mice: Foxp3-Fusion-GFP versus Foxp3-ires-GFP.

description_full:
[cell repeats an earlier one in this file: 120 characters]


description_brief: Genes up-regulated in hematopoietic stem cells versus lymphoid primed multipotent progenitors.
systematic_name: M8828
exact_source: GSE37301_2593_200_UP
source_species_code: MM
GEO_id: GSE37301
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  Expression profiling of Rag2-deficient Ets1++ and Rag2-deficient Ets1-- mature NK cells and WT bone marrow progenitors, WT T cells, and WT Pro B cells


systematic_name: M8833
exact_source: GSE37301_2619_200_DN
source_species_code: MM
GEO_id: GSE37301
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in granulocyte-monocyte progenitor versus RAG2 [GeneID=5897] knockout NK cells.

description_full:
[cell repeats an earlier one in this file: 150 characters]


systematic_name: M8844
exact_source: GSE37301_2620_200_UP
source_species_code: MM
GEO_id: GSE37301
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in NK cells: RAG2 [GeneID=5897] knockout versus RAG2 and ETS1 [GeneID=5897;2113] knockout.

description_full:
[cell repeats an earlier one in this file: 150 characters]


systematic_name: M8846
exact_source: GSE37301_2620_200_DN
source_species_code: MM
GEO_id: GSE37301
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in NK cells: RAG2 [GeneID=5897] knockout versus RAG2 and ETS1 [GeneID=5897;2113] knockout.

description_full:
[cell repeats an earlier one in this file: 150 characters]


systematic_name: M8860
exact_source: GSE37301_2608_200_UP
source_species_code: MM
GEO_id: GSE37301
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in lymphoid primed multipotent progenitors versus granulocyte-monocyte progenitors.

description_full:
[cell repeats an earlier one in this file: 150 characters]


systematic_name: M8861
exact_source: GSE37301_2608_200_DN
source_species_code: MM
GEO_id: GSE37301
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in lymphoid primed multipotent progenitors versus granulocyte-monocyte progenitors.

description_full:
[cell repeats an earlier one in this file: 150 characters]


systematic_name: M8863
exact_source: GSE37301_2609_200_UP
source_species_code: MM
GEO_id: GSE37301
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in lymphoid primed multipotent progenitors versus RAG2 [GeneID=5897] knockout NK cells.

description_full:
[cell repeats an earlier one in this file: 150 characters]


systematic_name: M8864
exact_source: GSE37301_2609_200_DN
source_species_code: MM
GEO_id: GSE37301
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in lymphoid primed multipotent progenitors versus RAG2 [GeneID=5897] knockout NK cells.

description_full:
[cell repeats an earlier one in this file: 150 characters]


systematic_name: M8908
exact_source: GSE32255_3066_200_UP
source_species_code: MM
GEO_id: GSE32255
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in dendritic cells: unstimulated wildtype versus KDM4D [GeneID=55693] knockdown (shRNA) stimulated by LPS.

description_full:
  In dendritic cells, expression of the H3K9me3 demethylase JmjD2d is upregulated by LPS stimulation. To identify genes whose induction by LPS depends on JmjD2d activity, we performed a microarray analysis of wild-type and JmjD2d-knockdown dendritic cells, before and after stimulation with LPS.


systematic_name: M8909
exact_source: GSE32255_3066_200_DN
source_species_code: MM
GEO_id: GSE32255
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in dendritic cells: unstimulated wildtype versus KDM4D [GeneID=55693] knockdown (shRNA) stimulated by LPS.

description_full:
  In dendritic cells, expression of the H3K9me3 demethylase JmjD2d is upregulated by LPS stimulation. To identify genes whose induction by LPS depends on JmjD2d activity, we performed a microarray analysis of wild-type and JmjD2d-knockdown dendritic cells, before and after stimulation with LPS.


systematic_name: M8915
exact_source: GSE34217_3218_200_DN
source_species_code: MM
GEO_id: GSE34217
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in act CD8 T cells: over-expressing MIR17HG [GeneID=407975] versus activated control.

description_full:
  During acute viral infections, effector CD8+ T cells differentiate into memory precursors or short-lived terminal effectors. miR-17-92a over-expression skews CD8+ effector cells to the terminal differentiation. We used microarray to identify the genes that are differentially expressed caused by miR-17-92a over-expression.


systematic_name: M8917
exact_source: GSE34217_3218_200_UP
source_species_code: MM
GEO_id: GSE34217
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in act CD8 T cells: over-expressing MIR17HG [GeneID=407975] versus activated control.

description_full:
  During acute viral infections, effector CD8+ T cells differentiate into memory precursors or short-lived terminal effectors. miR-17-92a over-expression skews CD8+ effector cells to the terminal differentiation. We used microarray to identify the genes that are differentially expressed caused by miR-17-92a over-expression.


systematic_name: M8918
exact_source: GSE37319_3055_200_UP
source_species_code: MM
GEO_id: GSE37319
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD44 low [GeneID=960] CD8 T cells: wildtype versus RC3H1 [GeneID=149041] knockout.

description_full:
  We used microarrays to detect the primary changes caused by the 'san' mutation in Roquin gene by comparing the gene expression profiles of naive (CD44lo) CD8+ T cell population.


systematic_name: M8919
exact_source: GSE37319_3055_200_DN
source_species_code: MM
GEO_id: GSE37319
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD44 low [GeneID=960] CD8 T cells: wildtype versus RC3H1 [GeneID=149041] knockout.

description_full:
  We used microarrays to detect the primary changes caused by the 'san' mutation in Roquin gene by comparing the gene expression profiles of naive (CD44lo) CD8+ T cell population.


description_brief: Genes down-regulated in CD4 [GeneID=920] T cells: Th1 versus Th17 enriched.
systematic_name: M8920
exact_source: GSE32901_3355_200_DN
source_species_code: HS
GEO_id: GSE32901
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  In this study, we examined differential gene expression in naïve human CD4+ T cells, as well as in effector Th1, Th17-negative and Th17-enriched CD4- T cell subsets. We observed a marked enrichment for increased gene expression in effector CD4+ T cells compared to naive CD4+ among immune-mediated disease oci genes. Within effector T cells, expression of disease-associated genes was increased in Th17-enriched compared to Th17-negative cells. We used microarray to examine the gene expresssion profile and level of human naïve, Th1 and effector T cell subsets.


description_brief: Genes up-regulated in T reg: wildtype versus HDAC9 [GeneID=9734] knockout.
systematic_name: M8934
exact_source: GSE36095_2870_200_UP
source_species_code: MM
GEO_id: GSE36095
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  Targeting histone/protein deacetylase (HDAC)-6, -9, or Sirtuin-1 (Sirt1) augments the suppressive functions of Foxp3+ T regulatory (Treg) cells, but it is unclear if this involves different mechanisms, such that combined inhibition would be beneficial. We compared the suppressive functions of Tregs from wild-type C57BL/6 mice or mice with global (HDAC6-/-, HDAC9-/-, dual HDAC6/9-/-) or conditional deletion (CD4-Cre or Foxp3-Cre and floxed Sirt1; GSE26425) alone, or after treatment with isoform-selective HDAC inhibitors (HDACi). We found the heat shock response was crucial in mediating the effects of HDAC6, but not Sirt1 inhibition. Furthermore, while HDAC6, HDAC9 and Sirt1 all deacetylate Foxp3, each has diverse effects on Foxp3 transcription, and loss of HDAC9 is associated with stabilization of Stat5 acetylation and its transcriptional activity. Targeting different HDAC can increase Treg function by multiple and additive mechanisms, indicating the therapeutic potential for combinations of HDACi in the management of autoimmunity and alloresponses post-transplant.


description_brief: Genes down-regulated in visceral adipose tissue of aged mice: T reg versus T conv.
systematic_name: M8937
exact_source: GSE37532_2847_200_DN
source_species_code: MM
GEO_id: GSE37532
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  We identified Pparg as a major orchestrator of the phenotype of adipose-tissue resident regulatory T cells (VAT Tregs). To establish the role of Pparg in shaping the VAT Tregs gene profile and cell dynamics, Tregs from lymph nodes and visceral adipose tissue of mice sufficient and deficient of Pparg expression in Tregs were double sorted for microarray analysis.


systematic_name: M8938
exact_source: GSE37532_2846_200_DN
source_species_code: MM
GEO_id: GSE37532
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in T conv cells from aged PPARG [GeneID=5468] knockout mice: visceral adipose tissue versus lymph node.

description_full:
  We identified Pparg as a major orchestrator of the phenotype of adipose-tissue resident regulatory T cells (VAT Tregs). To establish the role of Pparg in shaping the VAT Tregs gene profile and cell dynamics, Tregs from lymph nodes and visceral adipose tissue of mice sufficient and deficient of Pparg expression in Tregs were double sorted for microarray analysis.


systematic_name: M8947
exact_source: GSE37532_2845_200_UP
source_species_code: MM
GEO_id: GSE37532
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in T reg cells from aged PPARG [GeneID=5468] knockout mice: visceral adipose tissue versus lymph node.

description_full:
[cell repeats an earlier one in this file: 364 characters]


systematic_name: M8948
exact_source: GSE37532_2845_200_DN
source_species_code: MM
GEO_id: GSE37532
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in T reg cells from aged PPARG [GeneID=5468] knockout mice: visceral adipose tissue versus lymph node.

description_full:
[cell repeats an earlier one in this file: 364 characters]


systematic_name: M8949
exact_source: GSE37532_2846_200_UP
source_species_code: MM
GEO_id: GSE37532
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in T conv cells from aged PPARG [GeneID=5468] knockout: visceral adipose tissue versus lymph node.

description_full:
[cell repeats an earlier one in this file: 364 characters]


systematic_name: M8952
exact_source: GSE37532_2853_200_UP
source_species_code: MM
GEO_id: GSE37532
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in T reg from lypmh nodes of elderly (retired breeder) mice: wildtype versus PPARG [GeneID=5468] knockout.

description_full:
[cell repeats an earlier one in this file: 364 characters]


systematic_name: M8953
exact_source: GSE37532_2853_200_DN
source_species_code: MM
GEO_id: GSE37532
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in T reg from lypmh nodes of elderly (retired breeder) mice: wildtype versus PPARG [GeneID=5468] knockout.

description_full:
[cell repeats an earlier one in this file: 364 characters]


systematic_name: M8954
exact_source: GSE37532_2854_200_UP
source_species_code: MM
GEO_id: GSE37532
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in T conv from lymph node of elderly (retired breeder) mice: wildtype versus PPARG [GeneID=5468] knockout.

description_full:
[cell repeats an earlier one in this file: 364 characters]


systematic_name: M8955
exact_source: GSE37532_2848_200_UP
source_species_code: MM
GEO_id: GSE37532
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in visceral adipose tissue from aged PPARG [GeneID=5468] knockout mice: T reg versus T conv.

description_full:
[cell repeats an earlier one in this file: 364 characters]


systematic_name: M8956
exact_source: GSE37532_2848_200_DN
source_species_code: MM
GEO_id: GSE37532
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in visceral adipose tissue from aged PPARG [GeneID=5468] knockout mice: T reg versus T conv.

description_full:
[cell repeats an earlier one in this file: 364 characters]


systematic_name: M8960
exact_source: GSE37532_2850_200_DN
source_species_code: MM
GEO_id: GSE37532
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in lymph node from aged PPARG [GeneID=5468] knockout mice: T reg versus T conv.

description_full:
[cell repeats an earlier one in this file: 364 characters]


systematic_name: M8961
exact_source: GSE37532_2851_200_UP
source_species_code: MM
GEO_id: GSE37532
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in T reg from visceral adipose tissue of aged mice: wildtype versus PPARG [GeneID=5468] knockout.

description_full:
[cell repeats an earlier one in this file: 364 characters]


systematic_name: M8962
exact_source: GSE37532_2851_200_DN
source_species_code: MM
GEO_id: GSE37532
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in T reg from visceral adipose tissue of aged mice: wildtype versus PPARG [GeneID=5468] knockout.

description_full:
[cell repeats an earlier one in this file: 364 characters]


systematic_name: M8964
exact_source: GSE37532_2852_200_UP
source_species_code: MM
GEO_id: GSE37532
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in T conv from visceral adipose tissue in aged mice: wildtype versus PPARG [GeneID=5468] knockout.

description_full:
[cell repeats an earlier one in this file: 364 characters]


systematic_name: M8966
exact_source: GSE37532_2852_200_DN
source_species_code: MM
GEO_id: GSE37532
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in T conv from visceral adipose tissue in aged mice: wildtype versus PPARG [GeneID=5468] knockout.

description_full:
[cell repeats an earlier one in this file: 364 characters]


systematic_name: M8967
exact_source: GSE37533_2859_200_DN
source_species_code: MM
GEO_id: GSE37533
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] over-expressing: FOXP3 [GeneID=50943] and PPARg1 form of PPARG [GeneID=5468] versus FOXP3 [GeneID=50943].

description_full:
  We identified Pparg as a major orchestrator of the phenotype of adipose-tissue resident regulatory T cells (VAT Tregs). To explore the contribution of Pparg1 and 2 in the generation of the VAT Tregs-specific gene signatures, CD4+FoxP3- T cells were transduced with Foxp3+/- Pparg1 (or Pparg2), treated with Pioglitazone or vehicle, and double sorted for microarray analysis.


systematic_name: M8968
exact_source: GSE37533_2860_200_UP
source_species_code: MM
GEO_id: GSE37533
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] over-expressing: FOXP3 [GeneID=50943] and PPARg2 form of PPARG [GeneID=5468] versus FOXP3 [GeneID=50943].

description_full:
  We identified Pparg as a major orchestrator of the phenotype of adipose-tissue resident regulatory T cells (VAT Tregs). To explore the contribution of Pparg1 and 2 in the generation of the VAT Tregs-specific gene signatures, CD4+FoxP3- T cells were transduced with Foxp3+/- Pparg1 (or Pparg2), treated with Pioglitazone or vehicle, and double sorted for microarray analysis.


systematic_name: M8969
exact_source: GSE37533_2860_200_DN
source_species_code: MM
GEO_id: GSE37533
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] over-expressing: FOXP3 [GeneID=50943] and PPARg2 form of PPARG [GeneID=5468] versus FOXP3 [GeneID=50943].

description_full:
  We identified Pparg as a major orchestrator of the phenotype of adipose-tissue resident regulatory T cells (VAT Tregs). To explore the contribution of Pparg1 and 2 in the generation of the VAT Tregs-specific gene signatures, CD4+FoxP3- T cells were transduced with Foxp3+/- Pparg1 (or Pparg2), treated with Pioglitazone or vehicle, and double sorted for microarray analysis.


systematic_name: M8970
exact_source: GSE37533_2861_200_UP
source_species_code: MM
GEO_id: GSE37533
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T cells treated with pioglitazone [PubChem=4829] and over-expressing: FOXP3 [GeneID=50943] and PPARg1 isoform of PPARG [GeneID=5468] versus FOXP3 [GeneID=50943] and PPARg2 form of PPARG [GeneID=5468].

description_full:
[cell repeats an earlier one in this file: 374 characters]


systematic_name: M8971
exact_source: GSE37533_2861_200_DN
source_species_code: MM
GEO_id: GSE37533
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T cells treated with pioglitazone [PubChem=4829] and over-expressing: FOXP3 [GeneID=50943] and PPARg1 isoform of PPARG [GeneID=5468] versus FOXP3 [GeneID=50943] and PPARg2 form of PPARG [GeneID=5468].

description_full:
[cell repeats an earlier one in this file: 374 characters]


systematic_name: M8972
exact_source: GSE37533_2862_200_UP
source_species_code: MM
GEO_id: GSE37533
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T cells treated with pioglitazone [PubChem=4829] and over-expressing: FOXP3 [GeneID=50943] and PPARg1 isoform of PPARG [GeneID=5468] versus FOXP3 [GeneID=50943].

description_full:
[cell repeats an earlier one in this file: 374 characters]


systematic_name: M8974
exact_source: GSE37533_2862_200_DN
source_species_code: MM
GEO_id: GSE37533
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T cells treated with pioglitazone [PubChem=4829] and over-expressing: FOXP3 [GeneID=50943] and PPARg1 isoform of PPARG [GeneID=5468] versus FOXP3 [GeneID=50943].

description_full:
[cell repeats an earlier one in this file: 374 characters]


systematic_name: M8975
exact_source: GSE37533_2863_200_UP
source_species_code: MM
GEO_id: GSE37533
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T cells treated with pioglitazone [PubChem=4829] and over-expressing: FOXP3 [GeneID=50943] and PPARg2 isoform of PPARG [GeneID=5468] versus FOXP3 [GeneID=50943].

description_full:
[cell repeats an earlier one in this file: 374 characters]


systematic_name: M8977
exact_source: GSE37533_2863_200_DN
source_species_code: MM
GEO_id: GSE37533
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T cells treated with pioglitazone [PubChem=4829] and over-expressing: FOXP3 [GeneID=50943] and PPARg2 isoform of PPARG [GeneID=5468] versus FOXP3 [GeneID=50943].

description_full:
[cell repeats an earlier one in this file: 374 characters]


systematic_name: M8978
exact_source: GSE37534_2864_200_UP
source_species_code: MM
GEO_id: GSE37534
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T cells over-expressing FOXP3 [GeneID=50943] and PPARg1 isoform of PPARG [GeneID=5468]: untreated versus GW1929 [PubChem=6518171].

description_full:
  Pioglitazone treatment of CD4+FoxP3- T cells transduced with Pparg and Foxp3 up-regulated a set of genes whose products have been implicated in lipid metabolism pathways. To verify the specificity of this treatment, we performed microarray analysis on Foxp3+Pparg1-transduced CD4+FoxP3- T cells after treatment with other PPARg agonists such as Rosiglitazone (TZD) and GW1929 (non-TZD).


systematic_name: M8979
exact_source: GSE37534_2864_200_DN
source_species_code: MM
GEO_id: GSE37534
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T cells over-expressing FOXP3 [GeneID=50943] and PPARg1 isoform of PPARG [GeneID=5468]: untreated versus GW1929 [PubChem=6518171].

description_full:
  Pioglitazone treatment of CD4+FoxP3- T cells transduced with Pparg and Foxp3 up-regulated a set of genes whose products have been implicated in lipid metabolism pathways. To verify the specificity of this treatment, we performed microarray analysis on Foxp3+Pparg1-transduced CD4+FoxP3- T cells after treatment with other PPARg agonists such as Rosiglitazone (TZD) and GW1929 (non-TZD).


systematic_name: M8980
exact_source: GSE37534_2865_200_UP
source_species_code: MM
GEO_id: GSE37534
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T cells over-expressing FOXP3 [GeneID=50943] and PPARg1 form of PPARG [GeneID=5468]: untreated versus pioglitazone [PubChem=4829].

description_full:
  Pioglitazone treatment of CD4+FoxP3- T cells transduced with Pparg and Foxp3 up-regulated a set of genes whose products have been implicated in lipid metabolism pathways. To verify the specificity of this treatment, we performed microarray analysis on Foxp3+Pparg1-transduced CD4+FoxP3- T cells after treatment with other PPARg agonists such as Rosiglitazone (TZD) and GW1929 (non-TZD).


systematic_name: M8982
exact_source: GSE37534_2865_200_DN
source_species_code: MM
GEO_id: GSE37534
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T cells over-expressing FOXP3 [GeneID=50943] and PPARg1 form of PPARG [GeneID=5468]: untreated versus pioglitazone [PubChem=4829].

description_full:
[cell repeats an earlier one in this file: 386 characters]


systematic_name: M8983
exact_source: GSE37534_2866_200_UP
source_species_code: MM
GEO_id: GSE37534
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T ceels over-expressing FOXP3 [GeneID=920] and PPARg1 isoform of PPARG [GeneID=5468]: untreated versus rosiglitazone [PubChem=77999].

description_full:
[cell repeats an earlier one in this file: 386 characters]


systematic_name: M8984
exact_source: GSE37534_2866_200_DN
source_species_code: MM
GEO_id: GSE37534
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T ceels over-expressing FOXP3 [GeneID=920] and PPARg1 isoform of PPARG [GeneID=5468]: untreated versus rosiglitazone [PubChem=77999].

description_full:
[cell repeats an earlier one in this file: 386 characters]


systematic_name: M8985
exact_source: GSE37534_2867_200_UP
source_species_code: MM
GEO_id: GSE37534
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T cells over-expressing FOXP3 [GeneID=50943] and PPARg1 isoform of PPARG [GeneID=5468]: GW1929 [PubChem=6518171] versus pioglitazone [PubChem=4829].

description_full:
[cell repeats an earlier one in this file: 386 characters]


systematic_name: M8986
exact_source: GSE37534_2867_200_DN
source_species_code: MM
GEO_id: GSE37534
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T cells over-expressing FOXP3 [GeneID=50943] and PPARg1 isoform of PPARG [GeneID=5468]: GW1929 [PubChem=6518171] versus pioglitazone [PubChem=4829].

description_full:
[cell repeats an earlier one in this file: 386 characters]


systematic_name: M8987
exact_source: GSE37534_2868_200_UP
source_species_code: MM
GEO_id: GSE37534
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T cells over-expressing FOXP3 [GeneID=50943] and PPARg1 isoform of PPARG [GeneID=5468]: GW1929 [PubChem=6518171] versus rosiglitazone [PubChem=77999].

description_full:
[cell repeats an earlier one in this file: 386 characters]


systematic_name: M8989
exact_source: GSE37534_2868_200_DN
source_species_code: MM
GEO_id: GSE37534
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T cells over-expressing FOXP3 [GeneID=50943] and PPARg1 isoform of PPARG [GeneID=5468]: GW1929 [PubChem=6518171] versus rosiglitazone [PubChem=77999].

description_full:
[cell repeats an earlier one in this file: 386 characters]


systematic_name: M8990
exact_source: GSE37534_2869_200_UP
source_species_code: MM
GEO_id: GSE37534
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T cells treated with rosiglitazone [PubChem=77999] and over-expressing: FOXP3 [GeneID=50943] and PPARg1 isoform of PPARG [GeneID=5468] versus FOXP3 [GeneID=50943] and PPARg2 isoform of PPARG [GeneID=5468].

description_full:
[cell repeats an earlier one in this file: 386 characters]


systematic_name: M8992
exact_source: GSE37534_2869_200_DN
source_species_code: MM
GEO_id: GSE37534
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T cells treated with rosiglitazone [PubChem=77999] and over-expressing: FOXP3 [GeneID=50943] and PPARg1 isoform of PPARG [GeneID=5468] versus FOXP3 [GeneID=50943] and PPARg2 isoform of PPARG [GeneID=5468].

description_full:
[cell repeats an earlier one in this file: 386 characters]


systematic_name: M8993
exact_source: GSE37533_2856_200_DN
source_species_code: MM
GEO_id: GSE37533
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T cells over-expressing FOXP3 [GeneID=50943] and Pparg2 isoform of PPARG [GeneID=5468]: untreated versus pioglitazone [PubChem=4829].

description_full:
[cell repeats an earlier one in this file: 374 characters]


systematic_name: M8994
exact_source: GSE37533_2857_200_UP
source_species_code: MM
GEO_id: GSE37533
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T cells over-expressing FOXP3 [GeneID=50943]: untreated versus pioglitazone [PubChem=4829].

description_full:
[cell repeats an earlier one in this file: 374 characters]


systematic_name: M8995
exact_source: GSE37533_2857_200_DN
source_species_code: MM
GEO_id: GSE37533
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T cells over-expressing FOXP3 [GeneID=50943]: untreated versus pioglitazone [PubChem=4829].

description_full:
[cell repeats an earlier one in this file: 374 characters]


systematic_name: M8996
exact_source: GSE37533_2858_200_UP
source_species_code: MM
GEO_id: GSE37533
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T cells over-expressing: FOXP3 [GeneID=50943] and PPARg1 isoform of PPARG [GeneID=5468] versus FOXP3 [GeneID=50943] and PPARg2 isoform of PPARG [GeneID=5468].

description_full:
[cell repeats an earlier one in this file: 374 characters]


systematic_name: M8997
exact_source: GSE37533_2858_200_DN
source_species_code: MM
GEO_id: GSE37533
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in PPARg1 Foxp3 transduced CD4 T cell versus PPARg2 Foxp3 transduced CD4 T cell.

description_full:
[cell repeats an earlier one in this file: 374 characters]


systematic_name: M9000
exact_source: GSE37533_2859_200_UP
source_species_code: MM
GEO_id: GSE37533
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] over-expressing: FOXP3 [GeneID=50943] and PPARg1 form of PPARG [GeneID=5468] versus FOXP3 [GeneID=50943].

description_full:
[cell repeats an earlier one in this file: 374 characters]


systematic_name: M9001
exact_source: GSE37533_2855_200_UP
source_species_code: MM
GEO_id: GSE37533
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T cells over-expressing FOXP3 [GeneID=50943] and Pparg1 isoform of PPARG [GeneID=5468]: untreated versus pioglitazone [PubChem=4829].

description_full:
[cell repeats an earlier one in this file: 374 characters]


systematic_name: M9002
exact_source: GSE37533_2855_200_DN
source_species_code: MM
GEO_id: GSE37533
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T cells over-expressing FOXP3 [GeneID=50943] and Pparg1 isoform of PPARG [GeneID=5468]: untreated versus pioglitazone [PubChem=4829].

description_full:
[cell repeats an earlier one in this file: 374 characters]


systematic_name: M9003
exact_source: GSE37533_2856_200_UP
source_species_code: MM
GEO_id: GSE37533
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T cells over-expressing FOXP3 [GeneID=50943] and Pparg2 isoform of PPARG [GeneID=5468]: untreated versus pioglitazone [PubChem=4829].

description_full:
[cell repeats an earlier one in this file: 374 characters]


systematic_name: M9004
exact_source: GSE37532_2854_200_DN
source_species_code: MM
GEO_id: GSE37532
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in T conv from lymph node of elderly (retired breeder) mice: wildtype versus PPARG [GeneID=5468] knockout.

description_full:
[cell repeats an earlier one in this file: 364 characters]


description_brief: Genes up-regulated in B lymphocytes: light zone versus dark zone.
systematic_name: M9005
exact_source: GSE38696_3171_200_UP
source_species_code: MM
GEO_id: GSE38696
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  Microarrays of gene expression in mouse germinal center light zone and dark zone B cells sorted according to the expression of cell surface molecules CD83 and CXCR4 We used microarray data to identify genes differentially expressed by B cells in the light and dark zones of germinal centers from mouse skin-draining lymph nodes 12 days after subcutaneous immunization with NP-OVA in alum.


description_brief: Genes up-regulated in B lymphocytes: light zone versus dark zone.
systematic_name: M9007
exact_source: GSE38697_3172_200_UP
source_species_code: HS
GEO_id: GSE38697
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  Microarrays of gene expression in human germinal center light zone and dark zone B cells sorted according to the expression of cell surface molecules CD83 and CXCR4 We used microarray data to identify genes differentially expressed by B cells in the light and dark zones of germinal centers from human tonsil specimens.


systematic_name: M9014
exact_source: GSE37563_3048_200_DN
source_species_code: MM
GEO_id: GSE37563
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] cells after immunization: wildtype versus CTLA4 [GeneID=1493] knockout.

description_full:
  CTLA-4 is thought to inhibit effector T cells both intrinsically, by competing with CD28 for B7 ligands, and extrinsically, through the action of regulatory T cells. We studied in vivo responses of normal and CTLA-4-deficient antigen-specific murine effector CD4+ T cells. In order to do these studies in a physiological model of immunity to foreign antigen, we transferred small numbers of congenically marked RAG2-deficient 5C.C7 T cells with either a normal or knockout allele of CTLA-4 into normal syngeneic B10.A recipient mice. The T cells were then activated by immunization with MCC peptide and LPS. To look for transcriptional signatures of negative regulation of T cell responses by CTLA-4, we used microarray analysis to compare transcripts in wild type and CTLA-4 KO 5C.C7 T cells four days after immunization. This is the first instance in which differences are observed in extent of accumulation of wild type and CTLA-4 KO 5C.C7 T cells.


systematic_name: M9015
exact_source: GSE37563_3048_200_UP
source_species_code: MM
GEO_id: GSE37563
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] cells after immunization: wildtype versus CTLA4 [GeneID=1493] knockout.

description_full:
  CTLA-4 is thought to inhibit effector T cells both intrinsically, by competing with CD28 for B7 ligands, and extrinsically, through the action of regulatory T cells. We studied in vivo responses of normal and CTLA-4-deficient antigen-specific murine effector CD4+ T cells. In order to do these studies in a physiological model of immunity to foreign antigen, we transferred small numbers of congenically marked RAG2-deficient 5C.C7 T cells with either a normal or knockout allele of CTLA-4 into normal syngeneic B10.A recipient mice. The T cells were then activated by immunization with MCC peptide and LPS. To look for transcriptional signatures of negative regulation of T cell responses by CTLA-4, we used microarray analysis to compare transcripts in wild type and CTLA-4 KO 5C.C7 T cells four days after immunization. This is the first instance in which differences are observed in extent of accumulation of wild type and CTLA-4 KO 5C.C7 T cells.


description_brief: Genes up-regulated in dendritic cells from: lymph node versus spleen.
systematic_name: M9017
exact_source: GSE39022_3505_200_UP
source_species_code: MM
GEO_id: GSE39022
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  Spleen and lymph node dendritic cells have a differential capacity do induce and retain iTreg cells. Therefore we performed a comparative analysis of the dendritic cells derived from these two compartments to identify the responsible genes


systematic_name: M9019
exact_source: GSE38681_2643_200_UP
source_species_code: MM
GEO_id: GSE38681
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in lymphoid primed multipotent progenitors: wildtype versus LYL1 [GeneID=4066] knockout.

description_full:
  We compared gene expression differences in Lyl-1 knockout vs wildtype LMPPs KO allele described in Pub Med ID: 21387538


systematic_name: M9020
exact_source: GSE38681_2643_200_DN
source_species_code: MM
GEO_id: GSE38681
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in lymphoid primed multipotent progenitors: wildtype versus LYL1 [GeneID=4066] knockout.

description_full:
  We compared gene expression differences in Lyl-1 knockout vs wildtype LMPPs KO allele described in Pub Med ID: 21387538


systematic_name: M9022
exact_source: GSE36527_2966_200_DN
source_species_code: MM
GEO_id: GSE36527
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD69- KRLG1- [GeneID=969;10219] T reg: SELL high [GeneID=6402] versus SELL low [GeneID=6402].

description_full:
  Thymic-derived natural T regulatory cells (nTregs) are characterized by functional and phenotypic heterogeneity. Recently, a small fraction of peripheral Tregs have been shown to express Klrg1, but it remains unclear the extent Klrg1 defines a unique Treg subset. Here we show that Klrg1+ Tregs represent a terminally differentiated Treg subset derived from Klrg1- Tregs. This subset is a recent antigen-responsive and a highly activated short-lived Treg population that expresses enhanced levels of Treg suppressive molecules and that preferentially resides within mucosal tissues. The development of Klrg1+ Tregs also requires extensive IL-2R signaling. This activity represents a distinct function for IL-2, independent from its contribution to Treg homeostasis and competitive fitness. These and other properties are analogous to terminally differentiated short-lived CD8+ T effector cells. Our findings suggest that an important pathway driving antigen-activated conventional T lymphocytes also operates for Tregs. Gene expression analysis was performed of this and other Treg subsets based on expression of CD62L, CD69, and Klrg1 to define the molecular properties of Klrg1+ Tregs and its relationship to other Treg subsets found in the peripheral immune tissues.


systematic_name: M9023
exact_source: GSE36527_2966_200_UP
source_species_code: MM
GEO_id: GSE36527
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD69- KRLG1- [GeneID=969;10219] T reg: SELL high [GeneID=6402] versus SELL low [GeneID=6402].

description_full:
  Thymic-derived natural T regulatory cells (nTregs) are characterized by functional and phenotypic heterogeneity. Recently, a small fraction of peripheral Tregs have been shown to express Klrg1, but it remains unclear the extent Klrg1 defines a unique Treg subset. Here we show that Klrg1+ Tregs represent a terminally differentiated Treg subset derived from Klrg1- Tregs. This subset is a recent antigen-responsive and a highly activated short-lived Treg population that expresses enhanced levels of Treg suppressive molecules and that preferentially resides within mucosal tissues. The development of Klrg1+ Tregs also requires extensive IL-2R signaling. This activity represents a distinct function for IL-2, independent from its contribution to Treg homeostasis and competitive fitness. These and other properties are analogous to terminally differentiated short-lived CD8+ T effector cells. Our findings suggest that an important pathway driving antigen-activated conventional T lymphocytes also operates for Tregs. Gene expression analysis was performed of this and other Treg subsets based on expression of CD62L, CD69, and Klrg1 to define the molecular properties of Klrg1+ Tregs and its relationship to other Treg subsets found in the peripheral immune tissues.


systematic_name: M9027
exact_source: GSE36527_2967_200_UP
source_species_code: MM
GEO_id: GSE36527
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in KLRG1- [GeneID=10219] T reg:SELL high CD69- [GeneID=6402;969] versus SELL low CD69+ [GeneID=6402;969].

description_full:
  Thymic-derived natural T regulatory cells (nTregs) are characterized by functional and phenotypic heterogeneity. Recently, a small fraction of peripheral Tregs have been shown to express Klrg1, but it remains unclear the extent Klrg1 defines a unique Treg subset. Here we show that Klrg1+ Tregs represent a terminally differentiated Treg subset derived from Klrg1- Tregs. This subset is a recent antigen-responsive and a highly activated short-lived Treg population that expresses enhanced levels of Treg suppressive molecules and that preferentially resides within mucosal tissues. The development of Klrg1+ Tregs also requires extensive IL-2R signaling. This activity represents a distinct function for IL-2, independent from its contribution to Treg homeostasis and competitive fitness. These and other properties are analogous to terminally differentiated short-lived CD8+ T effector cells. Our findings suggest that an important pathway driving antigen-activated conventional T lymphocytes also operates for Tregs. Gene expression analysis was performed of this and other Treg subsets based on expression of CD62L, CD69, and Klrg1 to define the molecular properties of Klrg1+ Tregs and its relationship to other Treg subsets found in the peripheral immune tissues.


systematic_name: M9028
exact_source: GSE36527_2967_200_DN
source_species_code: MM
GEO_id: GSE36527
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in KLRG1- [GeneID=10219] T reg:SELL high CD69- [GeneID=6402;969] versus SELL low CD69+ [GeneID=6402;969].

description_full:
[cell repeats an earlier one in this file: 1269 characters]


systematic_name: M9029
exact_source: GSE36527_2968_200_DN
source_species_code: MM
GEO_id: GSE36527
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in KLRG1- SELL low [GeneID=10219;6402] T reg: CD69- [GeneID=969] versus CD69+ [GeneID=969].

description_full:
[cell repeats an earlier one in this file: 1269 characters]


systematic_name: M9030
exact_source: GSE36527_2968_200_UP
source_species_code: MM
GEO_id: GSE36527
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in KLRG1- SELL low [GeneID=10219;6402] T reg: CD69- [GeneID=969] versus CD69+ [GeneID=969].

description_full:
[cell repeats an earlier one in this file: 1269 characters]


systematic_name: M9031
exact_source: GSE33162_3527_200_DN
source_species_code: MM
GEO_id: GSE33162
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in macrophages with heterozygous knockout of HDAC3 [GeneID=8841]: untreated versus LPS.

description_full:
  Pan-Hdac inhibitors (HDACi) are endowed with a potent anti-inflammatory activity, but the relative role of each of the eleven Hdac proteins sensitive to HDACi to the inflammatory gene expression program is unknown. Using an integrated genomic approach we found that Hdac3-deficient macrophages are unable to activate almost half of the inflammatory gene expression program when stimulated with lipopolysaccharide (LPS). A large part of the activation defect is due to loss of basal and LPS-inducible expression of IFNb, which in basal cells maintains Stat1 protein levels, and after stimulation acts in an autocrine/paracrine manner to promote a secondary wave of Stat1-dependent gene expression. We show that loss of Hdac3-mediated repression of nuclear receptors leads to hyperacetylation of thousands of genomic sites and associated gene derepression. The upregulation of the constitutively expressed prostaglandin endoperoxide synthase, Ptgs1 (Cox-1), has a causative role in the phenotype, since its chemical inhibition reverts the Ifnb activation defect. These data may have relevance for the use of selective Hdac inhibitors as anti-inflammatory agents.


systematic_name: M9035
exact_source: GSE33162_3527_200_UP
source_species_code: MM
GEO_id: GSE33162
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in macrophages with heterozygous knockout of HDAC3 [GeneID=8841]: untreated versus LPS.

description_full:
  Pan-Hdac inhibitors (HDACi) are endowed with a potent anti-inflammatory activity, but the relative role of each of the eleven Hdac proteins sensitive to HDACi to the inflammatory gene expression program is unknown. Using an integrated genomic approach we found that Hdac3-deficient macrophages are unable to activate almost half of the inflammatory gene expression program when stimulated with lipopolysaccharide (LPS). A large part of the activation defect is due to loss of basal and LPS-inducible expression of IFNb, which in basal cells maintains Stat1 protein levels, and after stimulation acts in an autocrine/paracrine manner to promote a secondary wave of Stat1-dependent gene expression. We show that loss of Hdac3-mediated repression of nuclear receptors leads to hyperacetylation of thousands of genomic sites and associated gene derepression. The upregulation of the constitutively expressed prostaglandin endoperoxide synthase, Ptgs1 (Cox-1), has a causative role in the phenotype, since its chemical inhibition reverts the Ifnb activation defect. These data may have relevance for the use of selective Hdac inhibitors as anti-inflammatory agents.


systematic_name: M9038
exact_source: GSE33162_3529_200_UP
source_species_code: MM
GEO_id: GSE33162
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in macrophages with knockout of HDAC3 [GeneID=8841]: heterozygous versus homozygous.

description_full:
[cell repeats an earlier one in this file: 1160 characters]


systematic_name: M9039
exact_source: GSE33162_3529_200_DN
source_species_code: MM
GEO_id: GSE33162
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in macrophages with knockout of HDAC3 [GeneID=8841]: heterozygous versus homozygous.

description_full:
[cell repeats an earlier one in this file: 1160 characters]


systematic_name: M9040
exact_source: GSE33162_3530_200_DN
source_species_code: MM
GEO_id: GSE33162
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in macrophages with knockout of HDAC3 [GeneID=8841] after LPS treatment: heterozygous versus homozygous.

description_full:
[cell repeats an earlier one in this file: 1160 characters]


systematic_name: M9041
exact_source: GSE33162_3530_200_UP
source_species_code: MM
GEO_id: GSE33162
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in macrophages with knockout of HDAC3 [GeneID=8841] after LPS treatment: heterozygous versus homozygous.

description_full:
[cell repeats an earlier one in this file: 1160 characters]


description_brief: Genes down-regulated in T reg: wildtype versus ADORA2A [GeneID=135].
systematic_name: M9042
exact_source: GSE34006_3358_200_DN
source_species_code: MM
GEO_id: GSE34006
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  The adenosine 2A receptor (A2AR) is expressed on regulatory T cells (Tregs), but the functional significance is currently unknown. We compared the gene expression between wild-type (WT) and A2AR knockout (KO) Tregs and between WT Tregs treated with vehicle or a selective A2AR agonist.


systematic_name: M9049
exact_source: GSE34006_3360_200_DN
source_species_code: MM
GEO_id: GSE34006
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in T reg: untreated ADORA2A [GeneID=135] knockout versus wildtype treated by ZM 241385 [PubChem=176407].

description_full:
[cell repeats an earlier one in this file: 285 characters]


systematic_name: M9051
exact_source: GSE34006_3360_200_UP
source_species_code: MM
GEO_id: GSE34006
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in T reg: untreated ADORA2A [GeneID=135] knockout versus wildtype treated by ZM 241385 [PubChem=176407].

description_full:
[cell repeats an earlier one in this file: 285 characters]


description_brief: Genes up-regulated in Ly6C monocytes: high versus low.
systematic_name: M9053
exact_source: GSE32034_3117_200_UP
source_species_code: MM
GEO_id: GSE32034
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  PPARγ is known for its anti-inflammatory actions in macrophages. However, which macrophage populations express PPARγ in vivo and how it regulates tissue homeostasis in the steady state and during inflammation is not completely understood. We show that lung and spleen macrophages constitutively expressed PPARγ, while other macrophage populations did not. Recruitment of monocytes to sites of inflammation was associated with induction of PPARγ as they differentiated to macrophages. Its absence in these macrophages led to failed resolution of inflammation, characterized by persistent, low-level recruitment of leukocytes. Conversely, PPARγ agonists supported an earlier cessation in leukocyte recruitment during resolution of acute inflammation and likewise suppressed monocyte recruitment to chronically inflamed atherosclerotic vessels. In the steady state, PPARγ deficiency in macrophages had no obvious impact in the spleen but profoundly altered cellular lipid homeostasis in lung macrophages. Reminiscent of pulmonary alveolar proteinosis, LysM-Cre x PPARγflox/flox mice displayed mild leukocytic inflammation in the steady-state lung and succumbed faster to mortality upon infection with S. pneumoniae. Surprisingly, this mortality was not due to overly exuberant inflammation, but instead to impaired bacterial clearance. Thus, in addition to its anti-inflammatory role in promoting resolution of inflammation, PPARγ sustains functionality in lung macrophages and thereby has a pivotal role in supporting pulmonary host defense.


systematic_name: M9059
exact_source: GSE32034_3120_200_UP
source_species_code: MM
GEO_id: GSE32034
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in monocytes treated by rosiglitazone [PubChem=77999]: Ly6C high versus Ly6C low.

description_full:
[cell repeats an earlier one in this file: 1539 characters]


systematic_name: M9062
exact_source: GSE32034_3120_200_DN
source_species_code: MM
GEO_id: GSE32034
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in monocytes treated by rosiglitazone [PubChem=77999]: Ly6C high versus Ly6C low.

description_full:
[cell repeats an earlier one in this file: 1539 characters]


description_brief: Genes down-regulated in T reg cells: wildtype versus GATA3 [GeneID=2625] knockout.
systematic_name: M9063
exact_source: GSE39864_2644_200_DN
source_species_code: MM
GEO_id: GSE39864
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  The transcription factor Foxp3 is indispensible for the differentiation and function of regulatory T cells (Treg cells). To gain insights into the molecular mechanisms of Foxp3 mediated gene expression we purified Foxp3 complexes and explored their composition. Biochemical and mass-spectrometric analyses revealed that Foxp3 forms multi-protein complexes of 400-800 kDa or larger and identified 361 associated proteins ~30% of which are transcription-related. Foxp3 directly regulates expression of a large proportion of the genes encoding its co-factors. Reciprocally, some transcription factor partners of Foxp3 facilitate its expression. Functional analysis of Foxp3 cooperation with one such partner, Gata3, provided further evidence for a network of transcriptional regulation afforded by Foxp3 and its associates to control distinct aspects of Treg cell biology. Gene expression profile of Treg specific knock-out of Gata3 vs. their littermate controls were analyzed to gain insight into Gata3 dependendent genes in Treg cells.


systematic_name: M9067
exact_source: GSE39152_2716_200_DN
source_species_code: MM
GEO_id: GSE39152
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in memory CD8 T cells: ITGAE- [GeneID=3682] from spleen versus ITGAE+ [GeneID=3682] from brain.

description_full:
  Tissue resident memory (Trm) represent a newly described memory T cell population. We have previously characterized a population of Trm that persists within the brain following acute virus infection. Although capable of providing marked protection against a subsequent local challenge, brain Trm do not undergo recall expansion following dissociation from the tissue. Furthermore, these Trm do not depend on the same survival factors as the circulating memory T cell pool as assessed either in vivo or in vitro. To gain greater insight into this population of cells we compared the gene-expression profiles of Trm isolated from the brain to circulating memory T cells isolated from the spleen following an acute virus infection. Trm displayed altered expression of genes involved in chemotaxis, expressed a distinct set of transcription factors and overexpressed several inhibitory receptors. Cumulatively, these data indicates that Trm are a distinct memory T cell population disconnected from the circulating memory T cell pool and displaying a unique molecular signature which likely results in optimal survival and function within their local environment.


systematic_name: M9071
exact_source: GSE39152_2714_200_DN
source_species_code: MM
GEO_id: GSE39152
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in memory CD8 T cells, ITGAE- [GeneID=3682] population: brain versus spleen sources.

description_full:
  Tissue resident memory (Trm) represent a newly described memory T cell population. We have previously characterized a population of Trm that persists within the brain following acute virus infection. Although capable of providing marked protection against a subsequent local challenge, brain Trm do not undergo recall expansion following dissociation from the tissue. Furthermore, these Trm do not depend on the same survival factors as the circulating memory T cell pool as assessed either in vivo or in vitro. To gain greater insight into this population of cells we compared the gene-expression profiles of Trm isolated from the brain to circulating memory T cells isolated from the spleen following an acute virus infection. Trm displayed altered expression of genes involved in chemotaxis, expressed a distinct set of transcription factors and overexpressed several inhibitory receptors. Cumulatively, these data indicates that Trm are a distinct memory T cell population disconnected from the circulating memory T cell pool and displaying a unique molecular signature which likely results in optimal survival and function within their local environment.


systematic_name: M9073
exact_source: GSE39152_2715_200_UP
source_species_code: MM
GEO_id: GSE39152
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in memory CD8 T cells from brain: ITGAE- [GeneID=3682] versus ITGAE+ [GeneID=3682].

description_full:
  Tissue resident memory (Trm) represent a newly described memory T cell population. We have previously characterized a population of Trm that persists within the brain following acute virus infection. Although capable of providing marked protection against a subsequent local challenge, brain Trm do not undergo recall expansion following dissociation from the tissue. Furthermore, these Trm do not depend on the same survival factors as the circulating memory T cell pool as assessed either in vivo or in vitro. To gain greater insight into this population of cells we compared the gene-expression profiles of Trm isolated from the brain to circulating memory T cells isolated from the spleen following an acute virus infection. Trm displayed altered expression of genes involved in chemotaxis, expressed a distinct set of transcription factors and overexpressed several inhibitory receptors. Cumulatively, these data indicates that Trm are a distinct memory T cell population disconnected from the circulating memory T cell pool and displaying a unique molecular signature which likely results in optimal survival and function within their local environment.


systematic_name: M9074
exact_source: GSE39152_2715_200_DN
source_species_code: MM
GEO_id: GSE39152
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in memory CD8 T cells from brain: ITGAE- [GeneID=3682] versus ITGAE+ [GeneID=3682].

description_full:
[cell repeats an earlier one in this file: 1159 characters]


systematic_name: M9075
exact_source: GSE39152_2714_200_UP
source_species_code: MM
GEO_id: GSE39152
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in memory CD8 T cells, ITGAE- [GeneID=3682] population: brain versus spleen sources.

description_full:
[cell repeats an earlier one in this file: 1159 characters]


systematic_name: M9076
exact_source: GSE39152_2716_200_UP
source_species_code: MM
GEO_id: GSE39152
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in memory CD8 T cells: ITGAE- [GeneID=3682] from spleen versus ITGAE+ [GeneID=3682] from brain.

description_full:
[cell repeats an earlier one in this file: 1159 characters]


systematic_name: M9077
exact_source: GSE35685_2633_200_UP
source_species_code: HS
GEO_id: GSE35685
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in the bone marrow CD34+ [GeneID=947] cells: CD38- [GeneID=952] versus MME+ [GeneID=4311].

description_full:
  Studies of adult human hematopoiesis have until now relied on the expression of CD10 to define lymphoid commitment. We report a novel lymphoid-primed population in human bone marrow that is generated from hematopoietic stem cells (HSC) prior to the onset of CD10 expression and B cell commitment, and is identified by high levels of the homing molecule L-selectin (CD62L). CD10-CD62Lhi progenitors have full lymphoid (B/T/NK) potential, and show reduced myeloid and absent erythroid potential. Genome-wide gene expression analysis demonstrates that the CD10-CD62Lhi population represents an intermediate stage of differentiation between CD34+CD38- HSC and CD34+lin-CD10+ progenitors marked by down-regulation of TAL1 and MPL, upregulation of E2A, CD3E and IL2RG expression, and absent B cell commitment or RAG1/2 expression. Immature CD34+CD1a- thymocytes are also CD62Lhi and L-selectin ligands are expressed at the cortico-medullary junction, suggesting a possible role for L-selectin in human thymic homing. These studies identify the earliest stage of lymphoid priming in human bone marrow.


systematic_name: M9079
exact_source: GSE35685_2633_200_DN
source_species_code: HS
GEO_id: GSE35685
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in the bone marrow CD34+ [GeneID=947] cells: CD38- [GeneID=952] versus MME+ [GeneID=4311].

description_full:
  Studies of adult human hematopoiesis have until now relied on the expression of CD10 to define lymphoid commitment. We report a novel lymphoid-primed population in human bone marrow that is generated from hematopoietic stem cells (HSC) prior to the onset of CD10 expression and B cell commitment, and is identified by high levels of the homing molecule L-selectin (CD62L). CD10-CD62Lhi progenitors have full lymphoid (B/T/NK) potential, and show reduced myeloid and absent erythroid potential. Genome-wide gene expression analysis demonstrates that the CD10-CD62Lhi population represents an intermediate stage of differentiation between CD34+CD38- HSC and CD34+lin-CD10+ progenitors marked by down-regulation of TAL1 and MPL, upregulation of E2A, CD3E and IL2RG expression, and absent B cell commitment or RAG1/2 expression. Immature CD34+CD1a- thymocytes are also CD62Lhi and L-selectin ligands are expressed at the cortico-medullary junction, suggesting a possible role for L-selectin in human thymic homing. These studies identify the earliest stage of lymphoid priming in human bone marrow.


systematic_name: M9080
exact_source: GSE35685_2634_200_UP
source_species_code: HS
GEO_id: GSE35685
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in the bone marrow CD34+ [GeneID=947] cells: MME- SELL+[GeneID=4311;6402] versus MME+ [GeneID=4311].

description_full:
  Studies of adult human hematopoiesis have until now relied on the expression of CD10 to define lymphoid commitment. We report a novel lymphoid-primed population in human bone marrow that is generated from hematopoietic stem cells (HSC) prior to the onset of CD10 expression and B cell commitment, and is identified by high levels of the homing molecule L-selectin (CD62L). CD10-CD62Lhi progenitors have full lymphoid (B/T/NK) potential, and show reduced myeloid and absent erythroid potential. Genome-wide gene expression analysis demonstrates that the CD10-CD62Lhi population represents an intermediate stage of differentiation between CD34+CD38- HSC and CD34+lin-CD10+ progenitors marked by down-regulation of TAL1 and MPL, upregulation of E2A, CD3E and IL2RG expression, and absent B cell commitment or RAG1/2 expression. Immature CD34+CD1a- thymocytes are also CD62Lhi and L-selectin ligands are expressed at the cortico-medullary junction, suggesting a possible role for L-selectin in human thymic homing. These studies identify the earliest stage of lymphoid priming in human bone marrow.


systematic_name: M9081
exact_source: GSE35685_2634_200_DN
source_species_code: HS
GEO_id: GSE35685
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in the bone marrow CD34+ [GeneID=947] cells: MME- SELL+[GeneID=4311;6402] versus MME+ [GeneID=4311].

description_full:
[cell repeats an earlier one in this file: 1094 characters]


systematic_name: M9083
exact_source: GSE35685_2632_200_UP
source_species_code: HS
GEO_id: GSE35685
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in the bone marrow CD34+ [GeneID=947] cells: CD38- [GeneID=952] versus MME- SELL+ [GeneID=4311;6402].

description_full:
[cell repeats an earlier one in this file: 1094 characters]


systematic_name: M9084
exact_source: GSE35685_2632_200_DN
source_species_code: HS
GEO_id: GSE35685
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in the bone marrow CD34+ [GeneID=947] cells: CD38- [GeneID=952] versus MME- SELL+ [GeneID=4311;6402].

description_full:
[cell repeats an earlier one in this file: 1094 characters]


description_brief: Genes up-regulated in CD4 T conv: control versus over-expression of IRF4 [GeneID=3662].
systematic_name: M9085
exact_source: GSE40274_1459_200_UP
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  The transcription factor FoxP3 partakes dominantly in the specification and function of FoxP3+ CD4+ T regulatory cells (Tregs), but is neither strictly necessary nor sufficient to determine the characteristic Treg transcriptional signature. Computational network inference and experimental testing assessed the contribution of several other transcription factors (TFs). Enforced expression of Helios or Xbp1 elicited specific signatures, but Eos, Irf4, Satb1, Lef1 and Gata1 elicited exactly the same outcome, synergizing with FoxP3 to activate most of the Treg signature, including key TFs, and enhancing FoxP3 occupancy at its genomic targets. Conversely, the Treg signature was robust to inactivation of any single cofactor. A redundant genetic switch thus locks-in the Treg phenotype, a model which accounts for several aspects of Treg physiology, differentiation and stability.


systematic_name: M9102
exact_source: GSE40274_1466_200_UP
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 T conv: control versus over-expression of IKZF4 and FOXP3 [GeneID=64375;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9104
exact_source: GSE40274_1466_200_DN
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 T conv: control versus over-expression of IKZF4 and FOXP3 [GeneID=64375;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9105
exact_source: GSE40274_1467_200_UP
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 T conv: control versus over-expression of PBX1 and FOXP3 [GeneID=5087;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9106
exact_source: GSE40274_1467_200_DN
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 T conv: control versus over-expression of PBX1 and FOXP3 [GeneID=5087;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9107
exact_source: GSE40274_1468_200_UP
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 T conv: control versus over-expression of GATA1 and FOXP3 [GeneID=2623;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9108
exact_source: GSE40274_1468_200_DN
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 T conv: control versus over-expression of GATA1 and FOXP3 [GeneID=2623;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9109
exact_source: GSE40274_1469_200_UP
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 T conv: control versus over-expression of LEF1 and FOXP3 [GeneID=51176;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9110
exact_source: GSE40274_1469_200_DN
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 T conv: control versus over-expression of LEF1 and FOXP3 [GeneID=51176;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9111
exact_source: GSE40274_1470_200_UP
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 T conv: control versus over-expression of IRF4 and FOXP3 [GeneID=3662;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9113
exact_source: GSE40274_1470_200_DN
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 T conv: control versus over-expression of IRF4 and FOXP3 [GeneID=3662;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9114
exact_source: GSE40274_1471_200_UP
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 T conv: control versus over-expression of SATB1 and FOXP3 [GeneID=6304;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9115
exact_source: GSE40274_1471_200_DN
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 T conv: control versus over-expression of SATB1 and FOXP3 [GeneID=6304;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9116
exact_source: GSE40274_1472_200_UP
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 T conv: control versus over-expression of XBP1 and FOXP3 [GeneID=7494;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9117
exact_source: GSE40274_1472_200_DN
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 T conv: control versus over-expression of XBP1 and FOXP3 [GeneID=7494;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9119
exact_source: GSE40274_1473_200_UP
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 T conv: control versus over-expression of IKZF2 and FOXP3 [GeneID=22807;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9120
exact_source: GSE40274_1473_200_DN
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 T conv: control versus over-expression of IKZF2 and FOXP3 [GeneID=22807;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9121
exact_source: GSE40274_1474_200_UP
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 T conv over-expressing: FOXP3 [GeneID=50943] versus IKZF4 and FOXP3 [GeneID=64375;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9122
exact_source: GSE40274_1474_200_DN
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 T conv over-expressing: FOXP3 [GeneID=50943] versus IKZF4 and FOXP3 [GeneID=64375;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9141
exact_source: GSE40274_1479_200_UP
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 T conv over-expressing: FOXP3 [GeneID=50943] versus SATB1 and FOXP3 [GeneID=6304;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9145
exact_source: GSE40274_1479_200_DN
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 T conv over-expressing: FOXP3 [GeneID=50943] versus SATB1 and FOXP3 [GeneID=6304;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9146
exact_source: GSE40274_1480_200_UP
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 T conv over-expressing: FOXP3 [GeneID=50943] versus XBP1 and FOXP3 [GeneID=7494;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9147
exact_source: GSE40274_1480_200_DN
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 T conv over-expressing: FOXP3 [GeneID=50943] versus XBP1 and FOXP3 [GeneID=7494;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9148
exact_source: GSE40274_1481_200_UP
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 T conv over-expressing: FOXP3 [GeneID=50943] versus IKZF2 and FOXP3 [GeneID=22807;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9149
exact_source: GSE40274_1481_200_DN
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 T conv over-expressing: FOXP3 [GeneID=50943] versus IKZF2 and FOXP3 [GeneID=22807;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9151
exact_source: GSE40274_1482_200_UP
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 T conv over-expressing: IKZF4 [GeneID=64375] versus IKZF4 and FOXP3 [GeneID=64375;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9153
exact_source: GSE40274_1482_200_DN
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 T conv over-expressing: IKZF4 [GeneID=64375] versus IKZF4 and FOXP3 [GeneID=64375;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9154
exact_source: GSE40274_1483_200_UP
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 T conv over-expressing: IRF4 [GeneID=3662] versus IRF4 and FOXP3 [GeneID=3662;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9155
exact_source: GSE40274_1483_200_DN
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 T conv over-expressing: IRF4 [GeneID=3662] versus IRF4 and FOXP3 [GeneID=3662;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9156
exact_source: GSE40274_1484_200_UP
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 T conv over-expressing SATB1 [GeneID=6304] versus SATB1 and FOX3P [GeneID=6304;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9157
exact_source: GSE40274_1484_200_DN
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 T conv over-expressing SATB1 [GeneID=6304] versus SATB1 and FOX3P [GeneID=6304;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9158
exact_source: GSE40274_1485_200_UP
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 T conv over-expressing LEF1 [GeneID=51176] versus LEF1 and FOX3P [GeneID=51176;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9159
exact_source: GSE40274_1485_200_DN
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 T conv over-expressing LEF1 [GeneID=51176] versus LEF1 and FOX3P [GeneID=51176;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9161
exact_source: GSE40274_1486_200_UP
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 T conv over-expressing XBP1 [GeneID=7494] versus XBP1 and FOX3P [GeneID=7494;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9163
exact_source: GSE40274_1486_200_DN
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 T conv over-expressing XBP1 [GeneID=7494] versus XBP1 and FOX3P [GeneID=7494;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9164
exact_source: GSE40274_1487_200_UP
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 T conv over-expressing GATA1 [GeneID=2623] versus GATA1 and FOX3P [GeneID=2623;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9165
exact_source: GSE40274_1487_200_DN
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 T conv over-expressing GATA1 [GeneID=2623] versus GATA1 and FOX3P [GeneID=2623;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9166
exact_source: GSE40274_1488_200_UP
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 T conv over-expressing IKZF2 [GeneID=22807] versus IKZF2 and FOX3P [GeneID=22807;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9168
exact_source: GSE40274_1488_200_DN
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 T conv over-expressing IKZF2 [GeneID=22807] versus IKZF2 and FOX3P [GeneID=22807;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9169
exact_source: GSE40277_2922_200_UP
source_species_code: MM
GEO_id: GSE40277
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T conv over-expressing: IKZF4 and LEF1 [GeneID=64375;52276] versus GATA1 and SATB1 [GeneID=6304] versus GATA1 and SATB1 [GeneID=6304;2623].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9170
exact_source: GSE40277_2922_200_DN
source_species_code: MM
GEO_id: GSE40277
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T conv over-expressing: IKZF4 and LEF1 [GeneID=64375;52276] versus GATA1 and SATB1 [GeneID=6304] versus GATA1 and SATB1 [GeneID=6304;2623].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9171
exact_source: GSE40277_2923_200_UP
source_species_code: MM
GEO_id: GSE40277
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T conv: over-expressing IKZF4 and LEF1 [GeneID=64375;52276] versus control.

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9173
exact_source: GSE40277_2923_200_DN
source_species_code: MM
GEO_id: GSE40277
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T conv: over-expressing IKZF4 and LEF1 [GeneID=64375;52276] versus control.

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9175
exact_source: GSE40277_2924_200_UP
source_species_code: MM
GEO_id: GSE40277
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T conv over-expressing: GATA1 and SATB1 [GeneID=6304;2623] versus control.

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9178
exact_source: GSE40277_2924_200_DN
source_species_code: MM
GEO_id: GSE40277
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T conv over-expressing: GATA1 and SATB1 [GeneID=6304;2623] versus control.

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9179
exact_source: GSE40274_1478_200_DN
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 T conv over-expressing: FOXP3 [GeneID=50943] versus IRF4 and FOXP3 [GeneID=3662;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9180
exact_source: GSE40274_1476_200_DN
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 T conv over-expressing FOXP3 [GeneID=50943] versus GATA1 and FOXP3 [GeneID=2623;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9181
exact_source: GSE40274_1475_200_UP
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 T conv over-expressing: FOXP3 [GeneID=50943] versus PBX1 and FOXP3 [GeneID=5087;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9184
exact_source: GSE40274_1475_200_DN
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 T conv over-expressing: FOXP3 [GeneID=50943] versus PBX1 and FOXP3 [GeneID=5087;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9186
exact_source: GSE40274_1476_200_UP
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 T conv over-expressing FOXP3 [GeneID=50943] versus GATA1 and FOXP3 [GeneID=2623;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9187
exact_source: GSE40274_1477_200_UP
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 T conv over-expressing: FOXP3 [GeneID=50943] versus LEF1 and FOXP3 [GeneID=51176;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9188
exact_source: GSE40274_1477_200_DN
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 T conv over-expressing: FOXP3 [GeneID=50943] versus LEF1 and FOXP3 [GeneID=51176;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


systematic_name: M9190
exact_source: GSE40274_1478_200_UP
source_species_code: MM
GEO_id: GSE40274
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 T conv over-expressing: FOXP3 [GeneID=50943] versus IRF4 and FOXP3 [GeneID=3662;50943].

description_full:
[cell repeats an earlier one in this file: 882 characters]


description_brief: Genes down-regulated in T reg: NRP1+ [GeneID=8829] versus NRP1- [GeneID=8829].
systematic_name: M9195
exact_source: GSE40441_2405_200_DN
source_species_code: MM
GEO_id: GSE40441
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  To compare subpopulations of Treg cells in wild type mice based upon Nrp1 Expression, differentiating nTreg and iTreg


description_brief: Genes up-regulated in T reg: induced versus total.
systematic_name: M9198
exact_source: GSE40443_2403_200_UP
source_species_code: MM
GEO_id: GSE40443
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  iTreg cells from Tbmc mLN mice treated with one week of 1% Oral Ova were compared to Total Treg from WT mice.


description_brief: Genes up-regulated in CD8 T cells: naïve versus day 8 after LCMV infection.
systematic_name: M9203
exact_source: GSE40666_3510_200_UP
source_species_code: MM
GEO_id: GSE40666
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  Type 1 IFNs can conditionally activate all of the signal transducers and activators of transcription molecules (STATs), including STAT4. The best-characterized signaling pathways use STAT1, however, and type 1 IFN inhibition of cell proliferation is STAT1 dependent. We report that type 1 IFNs can basally stimulate STAT1- and STAT4- dependent effects in CD8 T cells, but that CD8 T cells responding to infections of mice with lymphocytic choriomenigitis virus have elevated STAT4 and lower STAT1 expression with significant consequences for modifying the effects of type 1 IFN exposure. The phenotype was associated with preferential type 1 IFN activation of STAT4 as compared to STAT1. Stimulation through the TCR induced elevated STAT4 expression, and STAT4 was required for peak expansion of antigen-specific CD8 T cells, low STAT1 levels, and resistance to type 1 IFN-mediated inhibition of proliferation. Thus, a mechanism is discovered for regulating the consequences of type 1 IFN exposure in CD8 T cells, with STAT4 acting as a key molecule in driving optimal antigen-specific responses and overcoming STAT1-dependent inhibition of proliferation.


systematic_name: M9208
exact_source: GSE40666_3511_200_UP
source_species_code: MM
GEO_id: GSE40666
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD8 T cells treated by interferon alpha: naïve versus day 8 after LCMV infection.

description_full:
[cell repeats an earlier one in this file: 1155 characters]


systematic_name: M9211
exact_source: GSE40666_3511_200_DN
source_species_code: MM
GEO_id: GSE40666
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD8 T cells treated by interferon alpha: naïve versus day 8 after LCMV infection.

description_full:
[cell repeats an earlier one in this file: 1155 characters]


systematic_name: M9214
exact_source: GSE40666_3514_200_UP
source_species_code: MM
GEO_id: GSE40666
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD8 T cells treated by interferon alpha: STAT1 [GeneID=6772] knockout versus STAT4 [GeneID=6775].

description_full:
[cell repeats an earlier one in this file: 1155 characters]


systematic_name: M9215
exact_source: GSE40666_3514_200_DN
source_species_code: MM
GEO_id: GSE40666
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD8 T cells treated by interferon alpha: STAT1 [GeneID=6772] knockout versus STAT4 [GeneID=6775].

description_full:
[cell repeats an earlier one in this file: 1155 characters]


systematic_name: M9216
exact_source: GSE40666_3515_200_UP
source_species_code: MM
GEO_id: GSE40666
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD8 T cells treated by inteferon alpha: wildtype versus STAT4 [GeneID=6775] knockout.

description_full:
[cell repeats an earlier one in this file: 1155 characters]


systematic_name: M9217
exact_source: GSE40666_3515_200_DN
source_species_code: MM
GEO_id: GSE40666
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD8 T cells treated by inteferon alpha: wildtype versus STAT4 [GeneID=6775] knockout.

description_full:
[cell repeats an earlier one in this file: 1155 characters]


systematic_name: M9220
exact_source: GSE40666_3517_200_UP
source_species_code: MM
GEO_id: GSE40666
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD8 T cells: STAT1 [GeneID=6772] knockout versus STAT4 [GeneID=6775] knockout.

description_full:
[cell repeats an earlier one in this file: 1155 characters]


systematic_name: M9222
exact_source: GSE40666_3517_200_DN
source_species_code: MM
GEO_id: GSE40666
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD8 T cells: STAT1 [GeneID=6772] knockout versus STAT4 [GeneID=6775] knockout.

description_full:
[cell repeats an earlier one in this file: 1155 characters]


systematic_name: M9229
exact_source: GSE40666_3507_200_DN
source_species_code: MM
GEO_id: GSE40666
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD8 T cells at day 8 after LCMV infection: untreated versus interferon alpha.

description_full:
[cell repeats an earlier one in this file: 1155 characters]


systematic_name: M9238
exact_source: GSE40225_3063_200_UP
source_species_code: MM
GEO_id: GSE40225
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in pancreatic CD8 T cells from mice with: type 1 diabetes mellitus versus healthy controls.

description_full:
  B7x (B7-H4 or B7S1) is the seventh member of the B7 family and the in vivo function remains largely unknown. Despite new genetic data linking the B7x gene with autoimmune diseases, how exactly it contributes to peripheral tolerance and autoimmunity is unclear. Here we showed that B7x protein was not detected on antigen-presenting cells or T cells in both human and mice, which is unique in the B7 family. As B7x protein is expressed in some peripheral cells such as pancreatic b cells, we utilized a CD8 T cell-mediated diabetes model (AI4ab) in which CD8 T cells recognize an endogenous self-antigen, and found that mice lacking B7x developed more severe diabetes than control AI4ab mice. Conversely, mice overexpressing B7x in the b cells (Rip-B7xAI4ab) were diabetes free. Furthermore, adoptive transfer of effector AI4ab CD8 T cells induced diabetes in control mice, but not in Rip-B7xAI4ab mice. Mechanistic studies revealed that pathogenic effector CD8 T cells were capable of migrating to the pancreas but failed to robustly destroy tissue when encountering local B7x in Rip-B7xAI4ab mice. Although AI4ab CD8 T cells in Rip-B7xAI4ab mice and AI4ab mice showed similar cytotoxic function, cell death, and global gene expression profiles, these cells had greater proliferation in AI4ab mice than in RIP-B7xAI4ab mice. These results suggest that B7x in nonlymphoid organs prevents peripheral autoimmunity partially through inhibiting proliferation of tissue-specific CD8 T cells and that local overexpression of B7x on pancreatic b cells is sufficient to abolish CD8 T cell-induced diabetes.


systematic_name: M9240
exact_source: GSE40225_3063_200_DN
source_species_code: MM
GEO_id: GSE40225
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in pancreatic CD8 T cells from mice with: type 1 diabetes mellitus versus healthy controls.

description_full:
  B7x (B7-H4 or B7S1) is the seventh member of the B7 family and the in vivo function remains largely unknown. Despite new genetic data linking the B7x gene with autoimmune diseases, how exactly it contributes to peripheral tolerance and autoimmunity is unclear. Here we showed that B7x protein was not detected on antigen-presenting cells or T cells in both human and mice, which is unique in the B7 family. As B7x protein is expressed in some peripheral cells such as pancreatic b cells, we utilized a CD8 T cell-mediated diabetes model (AI4ab) in which CD8 T cells recognize an endogenous self-antigen, and found that mice lacking B7x developed more severe diabetes than control AI4ab mice. Conversely, mice overexpressing B7x in the b cells (Rip-B7xAI4ab) were diabetes free. Furthermore, adoptive transfer of effector AI4ab CD8 T cells induced diabetes in control mice, but not in Rip-B7xAI4ab mice. Mechanistic studies revealed that pathogenic effector CD8 T cells were capable of migrating to the pancreas but failed to robustly destroy tissue when encountering local B7x in Rip-B7xAI4ab mice. Although AI4ab CD8 T cells in Rip-B7xAI4ab mice and AI4ab mice showed similar cytotoxic function, cell death, and global gene expression profiles, these cells had greater proliferation in AI4ab mice than in RIP-B7xAI4ab mice. These results suggest that B7x in nonlymphoid organs prevents peripheral autoimmunity partially through inhibiting proliferation of tissue-specific CD8 T cells and that local overexpression of B7x on pancreatic b cells is sufficient to abolish CD8 T cell-induced diabetes.


systematic_name: M9241
exact_source: GSE20727_3545_200_UP
source_species_code: MM
GEO_id: GSE20727
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in dendritic cells: 2,4-dinitrofluorobenzene (DNFB) [PubChem=6264] versus diphenyleneiodonium (DPI) [PubChem=2733504].

description_full:
  Identification of ROS induced genes on dendritic cells Dendritic cells were incubated for 15 min with or without a ROS inhibitor (DPI), washed extensively and incubated for 30 min with a chemical allergen (DNFB), hydrogen peroxide, and vehicle alone in HBSS containing DPI or vehicle. After washed extensively, the samples were post-incubated for 5.5 h with DNFB, hydrogen peroxide, or vehicle in complete culture medium containing DPI or vehicle.


systematic_name: M9242
exact_source: GSE20727_3543_200_DN
source_species_code: MM
GEO_id: GSE20727
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in dendritic cells: untreated versus diphenyleneiodonium (DPI) [PubChem=2733504].

description_full:
  Identification of ROS induced genes on dendritic cells Dendritic cells were incubated for 15 min with or without a ROS inhibitor (DPI), washed extensively and incubated for 30 min with a chemical allergen (DNFB), hydrogen peroxide, and vehicle alone in HBSS containing DPI or vehicle. After washed extensively, the samples were post-incubated for 5.5 h with DNFB, hydrogen peroxide, or vehicle in complete culture medium containing DPI or vehicle.


systematic_name: M9244
exact_source: GSE20727_3543_200_UP
source_species_code: MM
GEO_id: GSE20727
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in dendritic cells: untreated versus diphenyleneiodonium (DPI) [PubChem=2733504].

description_full:
[cell repeats an earlier one in this file: 447 characters]


systematic_name: M9247
exact_source: GSE20727_3544_200_DN
source_species_code: MM
GEO_id: GSE20727
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in dendritic cells: control versus 2,4-dinitrofluorobenzene (DNFB) [PubChem=6264] and diphenyleneiodonium (DPI) [PubChem=2733504].

description_full:
[cell repeats an earlier one in this file: 447 characters]


systematic_name: M9248
exact_source: GSE20727_3547_200_DN
source_species_code: MM
GEO_id: GSE20727
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in dendritic cells: diphenyleneiodonium (DPI) [PubChem=2733504] versus DPI and 2,4-dinitrofluorobenzene (DNFB) [PubChem=6264].

description_full:
[cell repeats an earlier one in this file: 447 characters]


systematic_name: M9249
exact_source: GSE20727_3541_200_DN
source_species_code: MM
GEO_id: GSE20727
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in dendritic cells: untreated versus 2,4-dinitrofluorobenzene (DNFB) [PubChem=6264].

description_full:
[cell repeats an earlier one in this file: 447 characters]


systematic_name: M9250
exact_source: GSE20727_3544_200_UP
source_species_code: MM
GEO_id: GSE20727
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in dendritic cells: control versus 2,4-dinitrofluorobenzene (DNFB) [PubChem=6264] and diphenyleneiodonium (DPI) [PubChem=2733504].

description_full:
[cell repeats an earlier one in this file: 447 characters]


systematic_name: M9252
exact_source: GSE20727_3547_200_UP
source_species_code: MM
GEO_id: GSE20727
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in dendritic cells: diphenyleneiodonium (DPI) [PubChem=2733504] versus DPI and 2,4-dinitrofluorobenzene (DNFB) [PubChem=6264].

description_full:
[cell repeats an earlier one in this file: 447 characters]


systematic_name: M9253
exact_source: GSE20727_3546_200_DN
source_species_code: MM
GEO_id: GSE20727
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in dendritic cells: hydrogen peroxide [PubChem=784] versus diphenyleneiodonium (DPI) [PubChem=2733504].

description_full:
[cell repeats an earlier one in this file: 447 characters]


systematic_name: M9254
exact_source: GSE20727_3541_200_UP
source_species_code: MM
GEO_id: GSE20727
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in dendritic cells: untreated versus 2,4-dinitrofluorobenzene (DNFB) [PubChem=6264].

description_full:
[cell repeats an earlier one in this file: 447 characters]


systematic_name: M9255
exact_source: GSE20727_3546_200_UP
source_species_code: MM
GEO_id: GSE20727
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in dendritic cells: hydrogen peroxide [PubChem=784] versus diphenyleneiodonium (DPI) [PubChem=2733504].

description_full:
[cell repeats an earlier one in this file: 447 characters]


systematic_name: M9256
exact_source: GSE20727_3545_200_DN
source_species_code: MM
GEO_id: GSE20727
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in dendritic cells: 2,4-dinitrofluorobenzene (DNFB) [PubChem=6264] versus diphenyleneiodonium (DPI) [PubChem=2733504].

description_full:
[cell repeats an earlier one in this file: 447 characters]


systematic_name: M9258
exact_source: GSE40068_2479_200_UP
source_species_code: MM
GEO_id: GSE40068
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CXCR5+ BCL6+ [GeneID=643;604] follicular helper T cells versus CXCR5- BCL6- CD4+ [GeneID=643;604;920] T cells.

description_full:
  T follicular helper (Tfh) cells play a pivotal role in germinal center reactions, which requires Bcl6 transcription factor. To analyze their relationships with other effector T cell lineages and their stability in vivo, we developed and analyzed a new Bcl6 reporter mouse alone or together with other lineage reporter systems. Assisted with genome-wide transcriptome analysis, we show substantial plasticity of T cell differentiation in the early phase of immune response. At this stage, CXCR5 appears to be expressed in a Bcl6-independent manner. Once Bcl6 is highly expressed, Tfh cells can persist in vivo and some of them develop into memory cells. Together, our results indicate Bcl6 as a bona fide marker for Tfh polarized program.


systematic_name: M9259
exact_source: GSE40068_2480_200_UP
source_species_code: MM
GEO_id: GSE40068
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CXCR5+ BCL6+ [GeneID=643;604] follicular helper T cells versus CXCR5+ BCL6- CD4+ [GeneID=643;604;920] T cells.

description_full:
  T follicular helper (Tfh) cells play a pivotal role in germinal center reactions, which requires Bcl6 transcription factor. To analyze their relationships with other effector T cell lineages and their stability in vivo, we developed and analyzed a new Bcl6 reporter mouse alone or together with other lineage reporter systems. Assisted with genome-wide transcriptome analysis, we show substantial plasticity of T cell differentiation in the early phase of immune response. At this stage, CXCR5 appears to be expressed in a Bcl6-independent manner. Once Bcl6 is highly expressed, Tfh cells can persist in vivo and some of them develop into memory cells. Together, our results indicate Bcl6 as a bona fide marker for Tfh polarized program.


systematic_name: M9260
exact_source: GSE40068_2480_200_DN
source_species_code: MM
GEO_id: GSE40068
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CXCR5+ BCL6+ [GeneID=643;604] follicular helper T cells versus CXCR5+ BCL6- CD4+ [GeneID=643;604;920] T cells.

description_full:
  T follicular helper (Tfh) cells play a pivotal role in germinal center reactions, which requires Bcl6 transcription factor. To analyze their relationships with other effector T cell lineages and their stability in vivo, we developed and analyzed a new Bcl6 reporter mouse alone or together with other lineage reporter systems. Assisted with genome-wide transcriptome analysis, we show substantial plasticity of T cell differentiation in the early phase of immune response. At this stage, CXCR5 appears to be expressed in a Bcl6-independent manner. Once Bcl6 is highly expressed, Tfh cells can persist in vivo and some of them develop into memory cells. Together, our results indicate Bcl6 as a bona fide marker for Tfh polarized program.


systematic_name: M9261
exact_source: GSE40068_2481_200_UP
source_species_code: MM
GEO_id: GSE40068
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CXCR5- BCL6- CD4+ [GeneID=643;604;920] T cells versus CXCR5+ BCL6- [GeneID=643;604] follicular helper T cells.

description_full:
[cell repeats an earlier one in this file: 737 characters]


systematic_name: M9262
exact_source: GSE40068_2479_200_DN
source_species_code: MM
GEO_id: GSE40068
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CXCR5+ BCL6+ [GeneID=643;604] follicular helper T cells versus CXCR5- BCL6- CD4+ [GeneID=643;604;920] T cells.

description_full:
[cell repeats an earlier one in this file: 737 characters]


systematic_name: M9263
exact_source: GSE40068_2481_200_DN
source_species_code: MM
GEO_id: GSE40068
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CXCR5- BCL6- CD4+ [GeneID=643;604;920] T cells versus CXCR5+ BCL6- [GeneID=643;604] follicular helper T cells.

description_full:
[cell repeats an earlier one in this file: 737 characters]


description_brief: Genes up-regulated in spleen B lymphocytes versus bone marrow plasma cells.
systematic_name: M9269
exact_source: GSE39916_3526_200_UP
source_species_code: MM
GEO_id: GSE39916
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  CD138+ B220- plasma cells were sorted from bone marrow and B220+ CD23+ mature follicular B cells were sorted from the spleens. Plasma cells were sorted from C57BL/6 mice 7 days after boosting with antigen, with mice first primed with an i.p. injection of KLH/IFA followed by boost at day 21 with KLH/PBS i.p. Mature B cells were sorted from antigen-naïve C57BL/6 mice. We compared expression profiles of plasma cells and mature B cells to identify differentially expressed transcripts.


description_brief: Genes up-regulated in germinal celter B lymphocytes: MYC- [GeneID=4609] versus MYC+ [GeneID=4609].
systematic_name: M9273
exact_source: GSE38304_2936_200_UP
source_species_code: MM
GEO_id: GSE38304
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  Germinal centers (GC) arise within B cell follicles upon antigenic challenge. In the dark zones (DZ) of GCs, B cells proliferate and hypermutate their immunoglobulin genes, and mutants with increased affinity are positively selected in the light zone (LZ) to either differentiate into plasma and memory cells, or re-enter the DZ for further refinement. However, the molecular circuits governing GC positive selection are not known. Here, we show that the GC reaction requires the biphasic regulation of c-MYC expression, involving its transient induction during early GC commitment, its repression by BCL6 in DZ B cells, and its re-induction in a subpopulation of positively selected LZ B cells destined to DZ re-entry. Accordingly, acute disruption of MYC function in vivo leads to GC collapse, indicating an essential role in GC physiology. These results have implications for our understanding of GC selection and the role of MYC deregulation in B cell lymphomas. We used microarrays to determine the global gene expression programs that distinguish MYC+ GC B cells from their MYC- negative counterparts.


systematic_name: M9274
exact_source: GSE38304_2936_200_DN
source_species_code: MM
GEO_id: GSE38304
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in germinal celter B lymphocytes: MYC- [GeneID=4609] versus MYC+ [GeneID=4609].

description_full:
  Germinal centers (GC) arise within B cell follicles upon antigenic challenge. In the dark zones (DZ) of GCs, B cells proliferate and hypermutate their immunoglobulin genes, and mutants with increased affinity are positively selected in the light zone (LZ) to either differentiate into plasma and memory cells, or re-enter the DZ for further refinement. However, the molecular circuits governing GC positive selection are not known. Here, we show that the GC reaction requires the biphasic regulation of c-MYC expression, involving its transient induction during early GC commitment, its repression by BCL6 in DZ B cells, and its re-induction in a subpopulation of positively selected LZ B cells destined to DZ re-entry. Accordingly, acute disruption of MYC function in vivo leads to GC collapse, indicating an essential role in GC physiology. These results have implications for our understanding of GC selection and the role of MYC deregulation in B cell lymphomas. We used microarrays to determine the global gene expression programs that distinguish MYC+ GC B cells from their MYC- negative counterparts.


systematic_name: M9275
exact_source: GSE39110_2723_200_DN
source_species_code: MM
GEO_id: GSE39110
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD8 T cells 3 days after immunization: control versus IL2 [GeneID=3558] treatment.

description_full:
  Much is known concerning the cellular and molecular basis for CD8+ T memory immune responses. Nevertheless, conditions that selectively support memory generation have remained elusive. Here we show that an immunization regimen that delivers TCR signals through a defined antigenic peptide, inflammatory signals through LPS, and growth and differentiation signals through the IL-2R initially favors antigen-specific CD8+ T cells to rapidly and substantially develop into tissue-residing T effector-memory cells by TCR transgenic OVA-specific OT-I CD8+ T cells. Amplified CD8+ T memory development depends upon a critical frequency of antigen-specific T cells and direct responsiveness to IL-2. A homologous prime-boost immunization protocol with transiently enhanced IL-2R signaling in normal mice led to persistent polyclonal antigen-specific CD8+ T cells that supported protective immunity to Listeria monocytogenes. These results identify a general approach for amplified T memory development that may be useful to optimize vaccines aimed at generating robust cell-mediated immunity. Gene expression analysis was performed for OT-I T cells on day 3 and day 5 after activation with ovalbumin and LPS in vivo with and without treatment with IL-2 using an agonists IL-2/anti-IL-2 complexes (IL2/Jes-6.1)


systematic_name: M9278
exact_source: GSE39110_2723_200_UP
source_species_code: MM
GEO_id: GSE39110
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD8 T cells 3 days after immunization: control versus IL2 [GeneID=3558] treatment.

description_full:
[cell repeats an earlier one in this file: 1302 characters]


systematic_name: M9281
exact_source: GSE39110_2725_200_UP
source_species_code: MM
GEO_id: GSE39110
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD8 T cells after immunization: day 3 versus day 6 and IL2 [GeneID=3558] treatment.

description_full:
[cell repeats an earlier one in this file: 1302 characters]


systematic_name: M9283
exact_source: GSE39110_2725_200_DN
source_species_code: MM
GEO_id: GSE39110
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD8 T cells after immunization: day 3 versus day 6 and IL2 [GeneID=3558] treatment.

description_full:
[cell repeats an earlier one in this file: 1302 characters]


systematic_name: M9284
exact_source: GSE39110_2726_200_UP
source_species_code: MM
GEO_id: GSE39110
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD8 T cells 6 days after immunization: control versus IL2 [GeneID=3558] treatment.

description_full:
[cell repeats an earlier one in this file: 1302 characters]


systematic_name: M9285
exact_source: GSE39110_2726_200_DN
source_species_code: MM
GEO_id: GSE39110
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD8 T cells 6 days after immunization: control versus IL2 [GeneID=3558] treatment.

description_full:
[cell repeats an earlier one in this file: 1302 characters]


systematic_name: M9286
exact_source: GSE36078_3660_200_UP
source_species_code: MM
GEO_id: GSE36078
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in Lung dendritic cell from Ad5 infection wildtype mice versus Lung dendritic cell from Ad5 inf IL-1R mice.

description_full:
  Discrimination between self vs. non-self and adequate response to infection and tissue damage are fundamental functions of the immune system. The rapid and global spread of known and emerging viruses is a testament that the timely detection of viral pathogens that reproduce within host cells, presents a formidable challenge to the immune system. To gain access to a proper reproductive niche, many pathogens travel via the host vasculature and therefore become exposed to humoral factors of the innate immune system. Although a cascade of coagulation factors plays a fundamental role in host defense for “living fossils” such as horseshoe crabs (Xiphosurida spp), the role of the coagulation system in activation of innate responses to pathogens in higher organisms remains unclear. When human type C adenovirus (HAdv) enters the circulation, 240 copies of coagulation factor X (FX) bind to the virus particle with picomolar affinity. Here, using molecular dynamics flexible fitting (MDFF) and high resolution cryo-electron microscopy (cryo-EM), we defined the interface between the HAdv5 hexon protein and FX at pseudo-atomic level. Based on this structural data, we introduced a single amino acid substitution, T424A, in the hexon that completely abrogated FX interaction with the virus. In vivo genome-wide transcriptional profiling revealed that FX-binding-ablated virus failed to activate a distinct network of the early response genes, whose expression depends on transcription factor NFKB1. Deconvolution of the signaling network responsible for early gene activation showed that the FX-HAdv complex triggers MyD88/TRIF/TRAF6 signaling upon activation of toll-like receptor 4 (TLR4) that serves as a principal sensor of FX-virus complex in vivo. Our study implicates host factor “decoration” of the virus as a mechanism to trigger innate immune sensor that respond to a misplacement of coagulation FX from the blood into intracellular macrophage compartments upon virus entry into the cell. Our results further the mounting evidence of evolutionary conservation between the coagulation system and innate immunity.


systematic_name: M9288
exact_source: GSE36078_3660_200_DN
source_species_code: MM
GEO_id: GSE36078
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in Lung dendritic cell from Ad5 infection wildtype mice versus Lung dendritic cell from Ad5 inf IL-1R mice.

description_full:
  Discrimination between self vs. non-self and adequate response to infection and tissue damage are fundamental functions of the immune system. The rapid and global spread of known and emerging viruses is a testament that the timely detection of viral pathogens that reproduce within host cells, presents a formidable challenge to the immune system. To gain access to a proper reproductive niche, many pathogens travel via the host vasculature and therefore become exposed to humoral factors of the innate immune system. Although a cascade of coagulation factors plays a fundamental role in host defense for “living fossils” such as horseshoe crabs (Xiphosurida spp), the role of the coagulation system in activation of innate responses to pathogens in higher organisms remains unclear. When human type C adenovirus (HAdv) enters the circulation, 240 copies of coagulation factor X (FX) bind to the virus particle with picomolar affinity. Here, using molecular dynamics flexible fitting (MDFF) and high resolution cryo-electron microscopy (cryo-EM), we defined the interface between the HAdv5 hexon protein and FX at pseudo-atomic level. Based on this structural data, we introduced a single amino acid substitution, T424A, in the hexon that completely abrogated FX interaction with the virus. In vivo genome-wide transcriptional profiling revealed that FX-binding-ablated virus failed to activate a distinct network of the early response genes, whose expression depends on transcription factor NFKB1. Deconvolution of the signaling network responsible for early gene activation showed that the FX-HAdv complex triggers MyD88/TRIF/TRAF6 signaling upon activation of toll-like receptor 4 (TLR4) that serves as a principal sensor of FX-virus complex in vivo. Our study implicates host factor “decoration” of the virus as a mechanism to trigger innate immune sensor that respond to a misplacement of coagulation FX from the blood into intracellular macrophage compartments upon virus entry into the cell. Our results further the mounting evidence of evolutionary conservation between the coagulation system and innate immunity.


systematic_name: M9290
exact_source: GSE36078_3659_200_DN
source_species_code: MM
GEO_id: GSE36078
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in Lung dendritic cell from untreated wildtype mice versus Lung dendritic cell from untreated IL-1R mice.

description_full:
[cell repeats an earlier one in this file: 2122 characters]


systematic_name: M9293
exact_source: GSE36078_3656_200_UP
source_species_code: MM
GEO_id: GSE36078
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in Lung dendritic cell from untreated wildtype mice versus Lung dendritic cell from Ad5 T424A hexon infection wildtype mice.

description_full:
[cell repeats an earlier one in this file: 2122 characters]


systematic_name: M9294
exact_source: GSE36078_3661_200_UP
source_species_code: MM
GEO_id: GSE36078
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in Lung dendritic cell from Ad5 T424A hexon infection wildtype mice versus Lung dendritic cell from Ad5 T424A hexon inf IL-1R mice.

description_full:
[cell repeats an earlier one in this file: 2122 characters]


systematic_name: M9295
exact_source: GSE36078_3661_200_DN
source_species_code: MM
GEO_id: GSE36078
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in Lung dendritic cell from Ad5 T424A hexon infection wildtype mice versus Lung dendritic cell from Ad5 T424A hexon inf IL-1R mice.

description_full:
[cell repeats an earlier one in this file: 2122 characters]


systematic_name: M9296
exact_source: GSE36078_3657_200_DN
source_species_code: MM
GEO_id: GSE36078
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in Lung dendritic cell from untreated IL-1R mice versus Lung dendritic cell from Ad5 inf IL-1R mice.

description_full:
[cell repeats an earlier one in this file: 2122 characters]


systematic_name: M9297
exact_source: GSE36078_3658_200_UP
source_species_code: MM
GEO_id: GSE36078
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in Lung dendritic cell from untreated IL-1R mice versus Lung dendritic cell from Ad5 T424A hexon inf IL-1R mice.

description_full:
[cell repeats an earlier one in this file: 2122 characters]


systematic_name: M9298
exact_source: GSE36078_3658_200_DN
source_species_code: MM
GEO_id: GSE36078
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in Lung dendritic cell from untreated IL-1R mice versus Lung dendritic cell from Ad5 T424A hexon inf IL-1R mice.

description_full:
[cell repeats an earlier one in this file: 2122 characters]


systematic_name: M9299
exact_source: GSE36078_3659_200_UP
source_species_code: MM
GEO_id: GSE36078
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in Lung dendritic cell from untreated wildtype mice versus Lung dendritic cell from untreated IL-1R mice.

description_full:
[cell repeats an earlier one in this file: 2122 characters]


systematic_name: M9301
exact_source: GSE36078_3657_200_UP
source_species_code: MM
GEO_id: GSE36078
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in Lung dendritic cell from untreated IL-1R mice versus Lung dendritic cell from Ad5 inf IL-1R mice.

description_full:
[cell repeats an earlier one in this file: 2122 characters]


systematic_name: M9302
exact_source: GSE36078_3656_200_DN
source_species_code: MM
GEO_id: GSE36078
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in Lung dendritic cell from untreated wildtype mice versus Lung dendritic cell from Ad5 T424A hexon infection wildtype mice.

description_full:
[cell repeats an earlier one in this file: 2122 characters]


description_brief: Genes down-regulated in CD4 [GeneID=920]: naïve versus FOXP3+ [GeneID=50943] T reg.
systematic_name: M9303
exact_source: GSE40685_2257_200_DN
source_species_code: MM
GEO_id: GSE40685
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  Regulatory T (Treg) cells, whose identity and function are defined by the transcription factor Foxp3, are indispensable for immune homeostasis. It is unclear whether Foxp3 exerts its Treg lineage specification function through active modification of the chromatin landscape and establishment of new enhancers or by exploiting a pre-existing enhancer landscape. Analysis of the chromatin accessibility of Foxp3-bound enhancers in Treg and Foxp3-negative T cells showed that Foxp3 was bound overwhelmingly to pre-accessible enhancers occupied by its cofactors in precursor cells or a structurally related predecessor. Furthermore, the bulk of Foxp3-bound Treg cell enhancers inaccessible in Foxp3- CD4+ cells became accessible upon T cell receptor activation prior to Foxp3 expression with only a small subset associated with several functionally important genes being exclusively Treg cell-specific. Thus, in a late cellular differentiation process Foxp3 defines Treg cell functionality in an “opportunistic” manner by largely exploiting the preformed enhancer network instead of establishing a new enhancer landscape.


systematic_name: M9306
exact_source: GSE40685_2259_200_UP
source_species_code: MM
GEO_id: GSE40685
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4: FOXP3+ [GeneID=50943] T reg versus FOXP3 [GeneID=50943] knockout T reg precursor.

description_full:
[cell repeats an earlier one in this file: 1117 characters]


systematic_name: M9308
exact_source: GSE40685_2259_200_DN
source_species_code: MM
GEO_id: GSE40685
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4: FOXP3+ [GeneID=50943] T reg versus FOXP3 [GeneID=50943] knockout T reg precursor.

description_full:
[cell repeats an earlier one in this file: 1117 characters]


description_brief: Genes down-regulated in follicular B cells versus day 40 germinal center B cells.
systematic_name: M9310
exact_source: GSE11961_2460_200_DN
source_species_code: MM
GEO_id: GSE11961
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  To obtain insight into the genetic basis of the increase of functional activity of memory B cells over time, we compared the gene expression profiles of day 7 and day 40 NP-specific/IgG1 memory B cells, GC B cells and plasma cells in immunized WT mice and naïve B cells, before and after activation in vitro.


systematic_name: M9333
exact_source: GSE11961_2461_200_UP
source_species_code: MM
GEO_id: GSE11961
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in follicular B cells versus those stimulated with anti-IgM and CD40 [GeneID=958] for 6h.

description_full:
[cell repeats an earlier one in this file: 308 characters]


systematic_name: M9335
exact_source: GSE11961_2461_200_DN
source_species_code: MM
GEO_id: GSE11961
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in follicular B cells versus those stimulated with anti-IgM and CD40 [GeneID=958] for 6h.

description_full:
[cell repeats an earlier one in this file: 308 characters]


systematic_name: M9342
exact_source: GSE28737_2490_200_UP
source_species_code: MM
GEO_id: GSE28737
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in marginal zone B lymphocytes: wildtype versus heterozygotic knockout of BCL6 [GeneID=604].

description_full:
  Bcl6 germline deletion causes a prominent inflammatory disease, owing to over-expression of Th2 cytokines, and affects the properties of B cells prior to immunization. Therefore we established the B cell-specific Bcl6 deletion mice and analyze the gene expression of naive B cells under physiological conditions.


systematic_name: M9344
exact_source: GSE28737_2490_200_DN
source_species_code: MM
GEO_id: GSE28737
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in marginal zone B lymphocytes: wildtype versus heterozygotic knockout of BCL6 [GeneID=604].

description_full:
  Bcl6 germline deletion causes a prominent inflammatory disease, owing to over-expression of Th2 cytokines, and affects the properties of B cells prior to immunization. Therefore we established the B cell-specific Bcl6 deletion mice and analyze the gene expression of naive B cells under physiological conditions.


systematic_name: M9348
exact_source: GSE28737_2492_200_UP
source_species_code: MM
GEO_id: GSE28737
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in marginal zone B lymphocytes with knockout of BCL6 [GeneID=604]: heterozygous versus homozygous.

description_full:
[cell repeats an earlier one in this file: 312 characters]


systematic_name: M9349
exact_source: GSE28737_2492_200_DN
source_species_code: MM
GEO_id: GSE28737
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in marginal zone B lymphocytes with knockout of BCL6 [GeneID=604]: heterozygous versus homozygous.

description_full:
[cell repeats an earlier one in this file: 312 characters]


systematic_name: M9354
exact_source: GSE28737_2494_200_UP
source_species_code: MM
GEO_id: GSE28737
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in heterozygous knockout of BCL6 [GeneID=604]: follicular versus marginal zone source.

description_full:
[cell repeats an earlier one in this file: 312 characters]


systematic_name: M9356
exact_source: GSE28737_2494_200_DN
source_species_code: MM
GEO_id: GSE28737
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in heterozygous knockout of BCL6 [GeneID=604]: follicular versus marginal zone source.

description_full:
[cell repeats an earlier one in this file: 312 characters]


systematic_name: M9380
exact_source: GSE28737_2489_200_UP
source_species_code: MM
GEO_id: GSE28737
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in follicular B lymphocytes with BCL6 [GeneID=604] knockout: heterozygotic versus homozygotic strains.

description_full:
[cell repeats an earlier one in this file: 312 characters]


systematic_name: M9383
exact_source: GSE28737_2487_200_DN
source_species_code: MM
GEO_id: GSE28737
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in follicular B lymphocytes: wildtype versus heterozygotic knockout of BCL6 [GeneID=604].

description_full:
[cell repeats an earlier one in this file: 312 characters]


systematic_name: M9385
exact_source: GSE28737_2489_200_DN
source_species_code: MM
GEO_id: GSE28737
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in follicular B lymphocytes with BCL6 [GeneID=604] knockout: heterozygotic versus homozygotic strains.

description_full:
[cell repeats an earlier one in this file: 312 characters]


systematic_name: M9391
exact_source: GSE28737_2487_200_UP
source_species_code: MM
GEO_id: GSE28737
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in follicular B lymphocytes: wildtype versus heterozygotic knockout of BCL6 [GeneID=604].

description_full:
[cell repeats an earlier one in this file: 312 characters]


description_brief: Genes up-regulated in Va14 invariant NKT cells: ZBTB7B [GeneID=51043] knockout versus wildtype.
systematic_name: M9397
exact_source: GSE34179_3503_200_UP
source_species_code: MM
GEO_id: GSE34179
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  We sought to identify genes regulated by the transcription factor Th-POK (Zbtb7b) in liver Va14i NKT cells, by RNA microarray analysis of global gene expression in Va14i NKT cells from mice homozygous for the Th-POK-inactivating hd point mutation as compared with the same cell population isolated from heterozygous or wild-type age-matched mice.


description_brief: Genes up-regulated in T reg: BCL6 [GeneID=604] knockout versus wildtype.
systematic_name: M9401
exact_source: GSE40493_2719_200_UP
source_species_code: MM
GEO_id: GSE40493
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  gene expression data from wild-type and Bcl6-/- regulatory T cells in order to find genes regulated by Bcl6 in Treg cells


systematic_name: M9404
exact_source: GSE40184_3228_200_DN
source_species_code: HS
GEO_id: GSE40184
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in peripheral blood monocytes (PBMC): healthy donors versus patients with HCV infection.

description_full:
  This study characterizes the effects of chronic Hepatitis C virus (HCV) infection on gene expression by analyzing blood samples from 10 treatment-naive HCV patients and 6 healthy volunteers. Differential expression analysis of microarray data from peripheral blood mononuclear cells (PBMCs) identified a 136 gene signature, including 66 genes elevated in infected individuals. Most of the up-regulated genes were associated with interferon (IFN) activity (including members of the OAS and MX families, ISG15 and IRF7), suggesting an ongoing immune response. This HCV signature was also found to be consistently enriched in many other viral infection and vaccination datasets. Validation of these genes was carried out using a second cohort composed of 5 HCV patients and 5 healthy volunteers, confirming the up-regulation of the IFN signature. In summary, this is the first study to directly compare blood transcriptional profiles from HCV patients with healthy controls. The results show that chronic HCV infection has a pronounced effect on gene expression in PBMCs of infected individuals, and significantly elevates the expression of a subset of interferon-stimulated genes.


systematic_name: M9405
exact_source: GSE40184_3228_200_UP
source_species_code: HS
GEO_id: GSE40184
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in peripheral blood monocytes (PBMC): healthy donors versus patients with HCV infection.

description_full:
  This study characterizes the effects of chronic Hepatitis C virus (HCV) infection on gene expression by analyzing blood samples from 10 treatment-naive HCV patients and 6 healthy volunteers. Differential expression analysis of microarray data from peripheral blood mononuclear cells (PBMCs) identified a 136 gene signature, including 66 genes elevated in infected individuals. Most of the up-regulated genes were associated with interferon (IFN) activity (including members of the OAS and MX families, ISG15 and IRF7), suggesting an ongoing immune response. This HCV signature was also found to be consistently enriched in many other viral infection and vaccination datasets. Validation of these genes was carried out using a second cohort composed of 5 HCV patients and 5 healthy volunteers, confirming the up-regulation of the IFN signature. In summary, this is the first study to directly compare blood transcriptional profiles from HCV patients with healthy controls. The results show that chronic HCV infection has a pronounced effect on gene expression in PBMCs of infected individuals, and significantly elevates the expression of a subset of interferon-stimulated genes.


description_brief: Genes up-regulated in CD8A [GeneID=925] dendritic cells versus NK cells.
systematic_name: M9406
exact_source: GSE39556_3192_200_UP
source_species_code: MM
GEO_id: GSE39556
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  The injection of the pathogen-associated molecular pattern Polyinosinic-polycytidylic acid (poly(I:C)) leads to the activation of various immune cells, including dendritic cells (DCs) and Natural Killer (NK) cells. This activation is due to different innate cytokines produced early after injection, in particular IFN-I. The objective of the study was to compare the pattern of expression of IFN-I stimulated genes between DC and NK cells. The project focused on a specific subset of conventional DC, CD8a DC, which responsiveness to IFN-I determines the capacity to activate CD8 T cells by cross-presentation of exogenous antigens. To identify the responses to IFN-I selectively induced in CD8a+ DC, we compared their gene expression profile to that of NK cells, using gene chips, before and after poly(I:C) stimulation.


description_brief: Genes up-regulated in DN3 thymocytes: wildtype versus TCF7 [GeneID=6932] knockout.
systematic_name: M9420
exact_source: GSE33292_2589_200_UP
source_species_code: MM
GEO_id: GSE33292
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  TCF-1 is an HMG family transcription factor which is known to be critical for T cell development. We discovered that it has a unique role in suppressing malignant transformation of developing thymocytes at early stages. We identified ID2 and LEF-1 as key TCF-1 target genens in tumor suppression. We used microarrays to detect gene expression changes in WT and TCF-1 deficient DN3 thymocytes as well as T cell lymphoma cells developed in TCF-1 KO mice.


systematic_name: M9424
exact_source: GSE33292_2590_200_UP
source_species_code: MM
GEO_id: GSE33292
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in wildtype DN3 thymocytes versus T cell lymphoma cells from TCF7 [GeneID=6932] knockout.

description_full:
[cell repeats an earlier one in this file: 452 characters]


systematic_name: M9427
exact_source: GSE33292_2590_200_DN
source_species_code: MM
GEO_id: GSE33292
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in wildtype DN3 thymocytes versus T cell lymphoma cells from TCF7 [GeneID=6932] knockout.

description_full:
[cell repeats an earlier one in this file: 452 characters]


description_brief: Genes down-regulated in T reg: in vivo versus in vitro.
systematic_name: M9428
exact_source: GSE35543_3049_200_DN
source_species_code: MM
GEO_id: GSE35543
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  Induced Treg (iTreg) cells are essential for tolerance and can be used therapeutically, yet their stability in vivo and mechanisms of suppression are unresolved. Here, we used a treatment model of colitis to examine the role of autologous IL-10 in iTreg cell function. Mice treated with IL-10+/+ iTreg cells in combination with IL-10–/– natural Treg (nTreg) cells survived and gained weight, even though iTreg cells were numerically disadvantaged and comprised just ~20% of all Treg cells in treated mice. Notably, ~85% of the transferred iTreg cells lost Foxp3 expression (ex-iTreg) but retained a portion of the iTreg transcriptome which failed to limit their pathogenic potential. The TCR repertoires of iTreg and ex-iTreg cells exhibited almost no overlap, which indicates that the two populations are clonally unrelated and maintained by different selective pressures. These data demonstrate a potent and critical role for iTreg cell produced IL-10 that can supplant the IL-10 produced by nTreg cells and compensate for the inherent instability of the iTreg population.


systematic_name: M9429
exact_source: GSE35543_3050_200_UP
source_species_code: MM
GEO_id: GSE35543
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in comparison between in vivo derived natural T reg (nTreg) and converted ex-iTreg (induced T reg that lost FOXP3 [GeneID=50943] expression).

description_full:
  Induced Treg (iTreg) cells are essential for tolerance and can be used therapeutically, yet their stability in vivo and mechanisms of suppression are unresolved. Here, we used a treatment model of colitis to examine the role of autologous IL-10 in iTreg cell function. Mice treated with IL-10+/+ iTreg cells in combination with IL-10–/– natural Treg (nTreg) cells survived and gained weight, even though iTreg cells were numerically disadvantaged and comprised just ~20% of all Treg cells in treated mice. Notably, ~85% of the transferred iTreg cells lost Foxp3 expression (ex-iTreg) but retained a portion of the iTreg transcriptome which failed to limit their pathogenic potential. The TCR repertoires of iTreg and ex-iTreg cells exhibited almost no overlap, which indicates that the two populations are clonally unrelated and maintained by different selective pressures. These data demonstrate a potent and critical role for iTreg cell produced IL-10 that can supplant the IL-10 produced by nTreg cells and compensate for the inherent instability of the iTreg population.


systematic_name: M9434
exact_source: GSE35543_3050_200_DN
source_species_code: MM
GEO_id: GSE35543
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in comparison between in vivo derived natural T reg (nTreg) and converted ex-iTreg (induced T reg that lost FOXP3 [GeneID=50943] expression).

description_full:
[cell repeats an earlier one in this file: 1074 characters]


systematic_name: M9436
exact_source: GSE35543_3051_200_DN
source_species_code: MM
GEO_id: GSE35543
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in comparison between in vitro derived induced T reg (iTreg) and converted ex iTreg.

description_full:
[cell repeats an earlier one in this file: 1074 characters]


systematic_name: M9437
exact_source: GSE35543_3051_200_UP
source_species_code: MM
GEO_id: GSE35543
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in comparison between in vitro derived induced T reg (iTreg) and converted ex iTreg.

description_full:
[cell repeats an earlier one in this file: 1074 characters]


description_brief: Genes up-regulated in normal T reg (nTreg): FOXO1 [GeneID=2308] versus wildtype.
systematic_name: M9439
exact_source: GSE40655_2890_200_UP
source_species_code: MM
GEO_id: GSE40655
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  Regulatory T (Treg) cells characterized by expression of the transcription factor forkhead box P3 (Foxp3) maintain immune homeostasis by suppressing self-destructive immune responses1-4. Foxp3 operates as a late acting differentiation factor controlling Treg cell homeostasis and function5, whereas the early Treg cell lineage commitment is regulated by the Akt kinase and the forkhead box O (Foxo) family of transcription factors6-10. However, whether Foxo proteins act beyond the Treg cell commitment stage to control Treg cell homeostasis and function remains largely unexplored. Here we show that Foxo1 is a pivotal regulator of Treg cell function. Treg cells express high amounts of Foxo1, and display reduced T-cell receptor-induced Akt activation, Foxo1 phosphorylation, and Foxo1 nuclear exclusion. Mice with Treg cell-specific deletion of Foxo1 develop a fatal inflammatory disorder similar in severity to Foxp3-deficient mice, but without the loss of Treg cells. Genome-wide analysis of Foxo1 binding sites reveals ~300 Foxo1-bound target genes, including the proinflammatory cytokine Ifng, that do not appear to be directly regulated by Foxp3. These findings demonstrate that the evolutionarily ancient Akt-Foxo1 signaling module controls a novel genetic program indispensable for Treg cell function.


description_brief: Genes down-regulated in splenocytes: control versus infected with Sendai virus.
systematic_name: M9443
exact_source: GSE24671_2560_200_DN
source_species_code: MM
GEO_id: GSE24671
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  The genome of vertebrates contains endogenous retroviruses (ERVs) that have resulted from ancestral infections by exogenous retroviruses. ERVs are germline encoded, transmitted in a Mendelian fashion and account for about 8% of the human and 9.9% of the murine genome, respectively1, 2. By spontaneous activation and reintegration ERVs may cause insertional mutagenesis and thus participate in the process of malignant transformation or progression of tumor growth3, 4. However, if the innate immune system is able to recognize and control ERVs has not yet been elucidated. Here we report that, in vitro, nucleic-acid sensing TLRs on dendritic cells are activated by retroviral RNA and DNA from infected cells in vitro. Infection of TLR competent wild type mice with murine leukemia virus (MuLV)-like ERV isolates results in non-canonical gene upregulation, independent of type I IFN. In vivo, TLR3, -7 and -9 triple deficient mice (TLR379-/-) and mice with non functional TLR3, 7 and 9 signaling due to a mutation in UNC93B develop spontaneous ERV-induced viremia. More importantly, in TLR379-/- mice ERV-induced viremia correlates with acute T cell lymphoblastic leukemia (T-ALL). Multiple independent TLR379-/- T cell leukemia lines produce infectious MuLV of endogenous origin. These cell lines display de novo retroviral integration into the Nup214 or Notch1 gene locus leading to gene dysregulation that is reminiscent of aberrant Nup214 and Notch1 expression in human T-ALLs5. Overall, our results demonstrate that in addition to their role in innate immune defense against exogenous pathogens, TLR3,-7, and -9 may be essential for the control of endogenous retroviral mediated T-cell lymphomagenesis.


systematic_name: M9449
exact_source: GSE41867_1604_200_UP
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD8 T effector cells during chronic infection with LCMV-Clone 13: day 8 versus day 15.

description_full:
  During acute viral infections, naïve CD8+ T cells differentiate into effector CD8+ T cells and, after viral control, into memory CD8+ T cells. Memory CD8+ T cells are highly functional, proliferate rapidly upon reinfection and persist long-term without antigen. In contrast, during chronic infections, CD8+ T cells become “exhausted” and have poor effector function, express multiple inhibitory receptors, possess low proliferative capacity, and cannot persist without antigen. To compare the development of functional memory T cells with poorly functional exhausted T cells, we generated longitudinal transcriptional profiles for each.


systematic_name: M9451
exact_source: GSE41867_1604_200_DN
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD8 T effector cells during chronic infection with LCMV-Clone 13: day 8 versus day 15.

description_full:
  During acute viral infections, naïve CD8+ T cells differentiate into effector CD8+ T cells and, after viral control, into memory CD8+ T cells. Memory CD8+ T cells are highly functional, proliferate rapidly upon reinfection and persist long-term without antigen. In contrast, during chronic infections, CD8+ T cells become “exhausted” and have poor effector function, express multiple inhibitory receptors, possess low proliferative capacity, and cannot persist without antigen. To compare the development of functional memory T cells with poorly functional exhausted T cells, we generated longitudinal transcriptional profiles for each.


systematic_name: M9452
exact_source: GSE41867_1605_200_UP
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD8 T cells during chronic infection with LCMV-Clone 13: effectors at day 15 versus exhausted at day 30.

description_full:
  During acute viral infections, naïve CD8+ T cells differentiate into effector CD8+ T cells and, after viral control, into memory CD8+ T cells. Memory CD8+ T cells are highly functional, proliferate rapidly upon reinfection and persist long-term without antigen. In contrast, during chronic infections, CD8+ T cells become “exhausted” and have poor effector function, express multiple inhibitory receptors, possess low proliferative capacity, and cannot persist without antigen. To compare the development of functional memory T cells with poorly functional exhausted T cells, we generated longitudinal transcriptional profiles for each.


systematic_name: M9453
exact_source: GSE41867_1605_200_DN
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD8 T cells during chronic infection with LCMV-Clone 13: effectors at day 15 versus exhausted at day 30.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9456
exact_source: GSE41867_1590_200_UP
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD8 T effector cells, acute infection with LCMV-Armstrong: day 6 versus day 8.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9457
exact_source: GSE41867_1590_200_DN
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD8 T effector cells, acute infection with LCMV-Armstrong: day 6 versus day 8.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9458
exact_source: GSE41867_1591_200_UP
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD8 T cells, acute infection with LCMV-Armstrong: effectors at day 6 versus memory at day 30.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9459
exact_source: GSE41867_1591_200_DN
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD8 T cells, acute infection with LCMV-Armstrong: effectors at day 6 versus memory at day 30.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9462
exact_source: GSE41867_1592_200_UP
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD8 T cells, acute infection with LCMV-Armstrong: effectors at day 8 versus memory at day 30.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9476
exact_source: GSE41867_1589_200_DN
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD8 T cells: naïve versus exhausted at day 30 chronic infection with LCMV-clone 13.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9477
exact_source: GSE41867_1596_200_DN
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD8 T effector cells at day 6 of chronic infection: LCMV-Armstrong versus LCMV-Clone 13.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9478
exact_source: GSE41867_1597_200_UP
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD8 T effector cells at day 8 of chronic infection: LCMV-Armstrong versus LCMV-Clone 13.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9479
exact_source: GSE41867_1597_200_DN
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD8 T effector cells at day 8 of chronic infection: LCMV-Armstrong versus LCMV-Clone 13.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9480
exact_source: GSE41867_1598_200_UP
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD8 T cells at day 30: memory cells after acute infection with LCMV-Armstrong versus exhausted cells during chronic infection with LCMV-Clone 13.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9482
exact_source: GSE41867_1598_200_DN
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD8 T cells at day 30: memory cells after acute infection with LCMV-Armstrong versus exhausted cells during chronic infection with LCMV-Clone 13.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9484
exact_source: GSE41867_1592_200_DN
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD8 T cells, acute infection with LCMV-Armstrong: effectors at day 8 versus memory at day 30.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9485
exact_source: GSE41867_1593_200_UP
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD8 T effector cells during chronic infection with LCMV-Clone 13: day 6 versus day 8.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9486
exact_source: GSE41867_1593_200_DN
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD8 T effector cells during chronic infection with LCMV-Clone 13: day 6 versus day 8.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9489
exact_source: GSE41867_1594_200_UP
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD8 T cells during chronic infection with LCMV-Clone 13: effectors at day 6 versus exhausted at day 30.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9490
exact_source: GSE41867_1594_200_DN
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD8 T cells during chronic infection with LCMV-Clone 13: effectors at day 6 versus exhausted at day 30.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9491
exact_source: GSE41867_1595_200_UP
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD8 T cells during chronic infection with LCMV-Clone 13: effectors at day 8 versus exhausted at day 30.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9492
exact_source: GSE41867_1595_200_DN
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD8 T cells during chronic infection with LCMV-Clone 13: effectors at day 8 versus exhausted at day 30.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9493
exact_source: GSE41867_1596_200_UP
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD8 T effector cells at day 6 of chronic infection: LCMV-Armstrong versus LCMV-Clone 13.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9495
exact_source: GSE41867_1583_200_UP
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD8 T cells: naïve versus effectors at day 6 after acute infection with LCMV-Armstrong.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9496
exact_source: GSE41867_1583_200_DN
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD8 T cells: naïve versus effectors at day 6 after acute infection with LCMV-Armstrong.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9497
exact_source: GSE41867_1584_200_UP
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD8 T cells: naïve versus effectors at day 8 after acute infection with LCMV-Armstrong.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9498
exact_source: GSE41867_1584_200_DN
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD8 T cells: naïve versus effectors at day 8 after acute infection with LCMV-Armstrong.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9499
exact_source: GSE41867_1585_200_UP
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD8 T cells: naïve versus effectors at day 15 after acute infection with LCMV-Armstrong.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9501
exact_source: GSE41867_1585_200_DN
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD8 T cells: naïve versus effectors at day 15 after acute infection with LCMV-Armstrong.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9502
exact_source: GSE41867_1586_200_UP
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD8 T cells: naïve versus memory at day 30 after acute infection with LCMV-Armstrong.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9504
exact_source: GSE41867_1586_200_DN
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD8 T cells: naïve versus memory at day 30 after acute infection with LCMV-Armstrong.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9505
exact_source: GSE41867_1587_200_UP
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD8 T cells: naïve versus effectors at day 8 chronic infection with LCMV-clone 13.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9506
exact_source: GSE41867_1587_200_DN
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD8 T cells: naïve versus effectors at day 8 chronic infection with LCMV-clone 13.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9507
exact_source: GSE41867_1588_200_UP
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD8 T cells: naïve versus effectors at day 15 chronic infection with LCMV-clone 13.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9508
exact_source: GSE41867_1588_200_DN
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD8 T cells: naïve versus effectors at day 15 chronic infection with LCMV-clone 13.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9509
exact_source: GSE41867_1589_200_UP
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD8 T cells: naïve versus exhausted at day 30 chronic infection with LCMV-clone 13.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9510
exact_source: GSE41867_1602_200_DN
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD8 T effector cells at day 15 of: acute infection with LCMV-Armstrong versus chronic infection with LCMV-Clone 13.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9512
exact_source: GSE41867_1603_200_UP
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD8 T effector cells during chronic infection with LCMV-Clone 13: day 6 versus day 15.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9513
exact_source: GSE41867_1603_200_DN
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD8 T effector cells during chronic infection with LCMV-Clone 13: day 6 versus day 15.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9515
exact_source: GSE41867_1599_200_DN
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD8 T effectors at acute infection with LCMV-Armstrong: day 6 versus day 15.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9519
exact_source: GSE41867_1600_200_DN
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD8 T effectors at acute infection with LCMV-Armstrong: day 8 versus day 15.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9521
exact_source: GSE41867_1601_200_DN
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD5 T cells at acute infection with LCMV-Armstrong: effectors at day 15 versus memory at day 30.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9522
exact_source: GSE41867_1602_200_UP
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD8 T effector cells at day 15 of: acute infection with LCMV-Armstrong versus chronic infection with LCMV-Clone 13.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9523
exact_source: GSE41867_1601_200_UP
source_species_code: MM
GEO_id: GSE41867
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD5 T cells at acute infection with LCMV-Armstrong: effectors at day 15 versus memory at day 30.

description_full:
[cell repeats an earlier one in this file: 636 characters]


systematic_name: M9527
exact_source: GSE41087_3902_200_UP
source_species_code: HS
GEO_id: GSE41087
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in activated CD4 [GeneID=920] T cells expressing: wildtype versus mutant form of FOXP3 [GeneID=50943].

description_full:
  Investigation of the role of FOXP3 in CD4+ T effector cells. FOXP3 is transiently upregulated in T effector cells under activation. This temporary expression in Teff cells is insufficient to suppress expression of reported targets of FOXP3 repressor activity. The role of FOXP3 in T effector cells remains unclear. We used microarray analysis to detail the differentially expressed genes between FOXP3 wild type and 2T>C(mut) clones and identified classes of up-regulated or down-regulated genes based upon FOXP3 expression.


systematic_name: M9528
exact_source: GSE41087_3902_200_DN
source_species_code: HS
GEO_id: GSE41087
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in activated CD4 [GeneID=920] T cells expressing: wildtype versus mutant form of FOXP3 [GeneID=50943].

description_full:
  Investigation of the role of FOXP3 in CD4+ T effector cells. FOXP3 is transiently upregulated in T effector cells under activation. This temporary expression in Teff cells is insufficient to suppress expression of reported targets of FOXP3 repressor activity. The role of FOXP3 in T effector cells remains unclear. We used microarray analysis to detail the differentially expressed genes between FOXP3 wild type and 2T>C(mut) clones and identified classes of up-regulated or down-regulated genes based upon FOXP3 expression.


description_brief: Genes down-regulated in skin: wildtype versus IL1R1 [GeneID=3554] knockout.
systematic_name: M9530
exact_source: GSE36826_2303_200_DN
source_species_code: MM
GEO_id: GSE36826
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  Neutrophil abscess formation is critical in innate immunity against many pathogens. Here, the mechanism of neutrophil abscess formation was investigated using a mouse model of Staphylococcus aureus cutaneous infection. Gene expression analysis of S. aureus-infected skin revealed that induction of neutrophil recruitment genes was largely dependent upon IL-1beta/IL-1R activation. Unexpectedly, using IL 1beta reporter mice, neutrophils were identified as the primary source of IL-1beta at the site of infection. Furthermore, IL-1beta-producing neutrophils were necessary and sufficient for abscess formation and bacterial clearance. S. aureus-induced IL 1beta production by neutrophils required TLR2, NOD2, FPRs and the ASC/NLRP3 inflammasome. Taken together, IL-1beta and neutrophil abscess formation during an infection are functionally, spatially and temporally linked as a consequence of direct IL-1beta production by neutrophils.


systematic_name: M9531
exact_source: GSE36826_2304_200_UP
source_species_code: MM
GEO_id: GSE36826
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in skin with IL1R1 [GeneID=3554] knockout: uninfected versus S. aureus infection.

description_full:
  Neutrophil abscess formation is critical in innate immunity against many pathogens. Here, the mechanism of neutrophil abscess formation was investigated using a mouse model of Staphylococcus aureus cutaneous infection. Gene expression analysis of S. aureus-infected skin revealed that induction of neutrophil recruitment genes was largely dependent upon IL-1beta/IL-1R activation. Unexpectedly, using IL 1beta reporter mice, neutrophils were identified as the primary source of IL-1beta at the site of infection. Furthermore, IL-1beta-producing neutrophils were necessary and sufficient for abscess formation and bacterial clearance. S. aureus-induced IL 1beta production by neutrophils required TLR2, NOD2, FPRs and the ASC/NLRP3 inflammasome. Taken together, IL-1beta and neutrophil abscess formation during an infection are functionally, spatially and temporally linked as a consequence of direct IL-1beta production by neutrophils.


systematic_name: M9532
exact_source: GSE36826_2304_200_DN
source_species_code: MM
GEO_id: GSE36826
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in skin with IL1R1 [GeneID=3554] knockout: uninfected versus S. aureus infection.

description_full:
  Neutrophil abscess formation is critical in innate immunity against many pathogens. Here, the mechanism of neutrophil abscess formation was investigated using a mouse model of Staphylococcus aureus cutaneous infection. Gene expression analysis of S. aureus-infected skin revealed that induction of neutrophil recruitment genes was largely dependent upon IL-1beta/IL-1R activation. Unexpectedly, using IL 1beta reporter mice, neutrophils were identified as the primary source of IL-1beta at the site of infection. Furthermore, IL-1beta-producing neutrophils were necessary and sufficient for abscess formation and bacterial clearance. S. aureus-induced IL 1beta production by neutrophils required TLR2, NOD2, FPRs and the ASC/NLRP3 inflammasome. Taken together, IL-1beta and neutrophil abscess formation during an infection are functionally, spatially and temporally linked as a consequence of direct IL-1beta production by neutrophils.


systematic_name: M9533
exact_source: GSE36826_2306_200_DN
source_species_code: MM
GEO_id: GSE36826
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in lesional skin biopsies after S. aureus infection: wildtype versus IL1R1 [GeneID=3554].

description_full:
[cell repeats an earlier one in this file: 935 characters]


systematic_name: M9536
exact_source: GSE36826_2306_200_UP
source_species_code: MM
GEO_id: GSE36826
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in lesional skin biopsies after S. aureus infection: wildtype versus IL1R1 [GeneID=3554].

description_full:
[cell repeats an earlier one in this file: 935 characters]


systematic_name: M9539
exact_source: GSE39382_2750_200_DN
source_species_code: MM
GEO_id: GSE39382
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in bone marrow-derived mast cells treated with IL3 [GeneID=3562]: control versus IL33 [GeneID=90865].

description_full:
  Interleukin-33 (IL-33) is elevated in afflicted tissues of patients with mast cell-dependent chronic allergic diseases. Based on its acute effects on mouse mast cells (MCs), IL-33 is thought to play a role in the pathogenesis of allergic disease through MC activation. However, the manifestations of chronic IL-33 exposure on human MC function, which best reflect the conditions associated with chronic allergic disease, are unknown. We now find that long-term exposure of human and mouse MCs to IL-33 results in a substantial reduction of MC activation in response to antigen. This reduction required >72 h exposure to IL-33 for onset and 1-2 wk for reversion following IL-33 removal. This hypo-responsive phenotype was determined to be a consequence of MyD88-dependent attenuation of signaling processes necessary for MC activation including antigen-mediated calcium mobilization and cytoskeletal reorganization; potentially as a consequence of down-regulation of the expression of PLCg1 and Hck. These findings suggest that IL-33 may play a protective, rather than a causative role in MC activation under chronic conditions and, furthermore, reveal regulated plasticity in the MC activation phenotype. The ability to down-regulate MC activation in this manner may provide alternative approaches for treatment of MC-driven disease.


systematic_name: M9540
exact_source: GSE39382_2750_200_UP
source_species_code: MM
GEO_id: GSE39382
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in bone marrow-derived mast cells treated with IL3 [GeneID=3562]: control versus IL33 [GeneID=90865].

description_full:
  Interleukin-33 (IL-33) is elevated in afflicted tissues of patients with mast cell-dependent chronic allergic diseases. Based on its acute effects on mouse mast cells (MCs), IL-33 is thought to play a role in the pathogenesis of allergic disease through MC activation. However, the manifestations of chronic IL-33 exposure on human MC function, which best reflect the conditions associated with chronic allergic disease, are unknown. We now find that long-term exposure of human and mouse MCs to IL-33 results in a substantial reduction of MC activation in response to antigen. This reduction required >72 h exposure to IL-33 for onset and 1-2 wk for reversion following IL-33 removal. This hypo-responsive phenotype was determined to be a consequence of MyD88-dependent attenuation of signaling processes necessary for MC activation including antigen-mediated calcium mobilization and cytoskeletal reorganization; potentially as a consequence of down-regulation of the expression of PLCg1 and Hck. These findings suggest that IL-33 may play a protective, rather than a causative role in MC activation under chronic conditions and, furthermore, reveal regulated plasticity in the MC activation phenotype. The ability to down-regulate MC activation in this manner may provide alternative approaches for treatment of MC-driven disease.


description_brief: Genes up-regulated in macrophages: resting versus stimulated by IL4 [GeneID=3565].
systematic_name: M9542
exact_source: GSE35435_3809_200_UP
source_species_code: MM
GEO_id: GSE35435
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  Analysis of alternative activation of macrophages at gene expression level. The study forms part of a wider study where we compare the effects of IL-4 in different human and mouse macrophages. Our results support the notion that in vitro culture conditions greatly affect the macrophage response to IL-4. Total RNA obtained from bone marrow derived macrophages upon exposure to 20 ng/ml of IL-4 for 18 hours.


description_brief: Genes down-regulated dendritic cells: Ly6G+ versus Ly6G-.
systematic_name: M9545
exact_source: GSE28408_3504_200_DN
source_species_code: MM
GEO_id: GSE28408
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  To investigate the functional properties of Ly6G+ DC, we employed GeneChip analysis to compare the gene expression profiles between Ly6G+ DC and Ly6C- DC.


systematic_name: M9548
exact_source: GSE41978_3690_200_DN
source_species_code: MM
GEO_id: GSE41978
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in KLRG1 low [GeneID=10219] CD8 T effector cells during infection: wildtype versus ID2 and BCL2L11 [GeneID=3398;10018] knockout.

description_full:
  CD8+ T cells play a crucial role in the clearance of intracellular pathogens through the generation of cytotoxic effector cells that eliminate infected cells and long-lived memory cells that provide enhanced protection against reinfection. We have previously shown that the inhibitor of E protein transcription factors, Id2, is necessary for accumulation of effector and memory CD8+ T cells during infection. Here we show that CD8+ T cells lacking Id2 did not generate a robust terminally-differentiated KLRG1hi effector population, but displayed a cell-surface phenotype and cytokine profile consistent with memory precursors, raising the question as to whether loss of Id2 impairs the differentiation and/or survival of effector-memory cells. We found that deletion of Bim rescued Id2-deficient CD8+ cell survival during infection. However, the dramatic reduction in KLRG1hi cells caused by loss of Id2 remained in the absence of Bim, such that Id2/Bim double-deficient cells form an exclusively KLRG1loCD127hi memory precursor population. Thus we describe a role for Id2 in both the survival and differentation of normal CD8+ effector and memory populations.


systematic_name: M9549
exact_source: GSE41978_3689_200_DN
source_species_code: MM
GEO_id: GSE41978
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in KLRG1 low [GeneID=10219] CD8 T effector cells during infection: wildtype versus ID2 [GeneID=3398].

description_full:
  CD8+ T cells play a crucial role in the clearance of intracellular pathogens through the generation of cytotoxic effector cells that eliminate infected cells and long-lived memory cells that provide enhanced protection against reinfection. We have previously shown that the inhibitor of E protein transcription factors, Id2, is necessary for accumulation of effector and memory CD8+ T cells during infection. Here we show that CD8+ T cells lacking Id2 did not generate a robust terminally-differentiated KLRG1hi effector population, but displayed a cell-surface phenotype and cytokine profile consistent with memory precursors, raising the question as to whether loss of Id2 impairs the differentiation and/or survival of effector-memory cells. We found that deletion of Bim rescued Id2-deficient CD8+ cell survival during infection. However, the dramatic reduction in KLRG1hi cells caused by loss of Id2 remained in the absence of Bim, such that Id2/Bim double-deficient cells form an exclusively KLRG1loCD127hi memory precursor population. Thus we describe a role for Id2 in both the survival and differentation of normal CD8+ effector and memory populations.


systematic_name: M9550
exact_source: GSE41978_3690_200_UP
source_species_code: MM
GEO_id: GSE41978
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in KLRG1 low [GeneID=10219] CD8 T effector cells during infection: wildtype versus ID2 and BCL2L11 [GeneID=3398;10018] knockout.

description_full:
  CD8+ T cells play a crucial role in the clearance of intracellular pathogens through the generation of cytotoxic effector cells that eliminate infected cells and long-lived memory cells that provide enhanced protection against reinfection. We have previously shown that the inhibitor of E protein transcription factors, Id2, is necessary for accumulation of effector and memory CD8+ T cells during infection. Here we show that CD8+ T cells lacking Id2 did not generate a robust terminally-differentiated KLRG1hi effector population, but displayed a cell-surface phenotype and cytokine profile consistent with memory precursors, raising the question as to whether loss of Id2 impairs the differentiation and/or survival of effector-memory cells. We found that deletion of Bim rescued Id2-deficient CD8+ cell survival during infection. However, the dramatic reduction in KLRG1hi cells caused by loss of Id2 remained in the absence of Bim, such that Id2/Bim double-deficient cells form an exclusively KLRG1loCD127hi memory precursor population. Thus we describe a role for Id2 in both the survival and differentation of normal CD8+ effector and memory populations.


systematic_name: M9551
exact_source: GSE41978_3688_200_UP
source_species_code: MM
GEO_id: GSE41978
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD8 T effector cells during infection: KLRG1 high [GeneID=10219] versus KLRG1 low [GeneID=10219].

description_full:
[cell repeats an earlier one in this file: 1161 characters]


systematic_name: M9552
exact_source: GSE41978_3688_200_DN
source_species_code: MM
GEO_id: GSE41978
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD8 T effector cells during infection: KLRG1 high [GeneID=10219] versus KLRG1 low [GeneID=10219].

description_full:
[cell repeats an earlier one in this file: 1161 characters]


systematic_name: M9553
exact_source: GSE41978_3689_200_UP
source_species_code: MM
GEO_id: GSE41978
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in KLRG1 low [GeneID=10219] CD8 T effector cells during infection: wildtype versus ID2 [GeneID=3398].

description_full:
[cell repeats an earlier one in this file: 1161 characters]


systematic_name: M9554
exact_source: GSE41978_3691_200_DN
source_species_code: MM
GEO_id: GSE41978
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in KLRG1 low [GeneID=10219] CD8 T effector cells during infection: wildtype versus BCL2L11 [GeneID=10018] knockout.

description_full:
[cell repeats an earlier one in this file: 1161 characters]


systematic_name: M9555
exact_source: GSE41978_3692_200_UP
source_species_code: MM
GEO_id: GSE41978
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in KLRG1 low [GeneID=10219] CD8 T effector cells during infection: ID2 [GeneID=3398] knockout versus ID2 and BCL2L11 [GeneID=3398;10018] knockout.

description_full:
[cell repeats an earlier one in this file: 1161 characters]


systematic_name: M9560
exact_source: GSE41978_3692_200_DN
source_species_code: MM
GEO_id: GSE41978
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in KLRG1 low [GeneID=10219] CD8 T effector cells during infection: ID2 [GeneID=3398] knockout versus ID2 and BCL2L11 [GeneID=3398;10018] knockout.

description_full:
[cell repeats an earlier one in this file: 1161 characters]


systematic_name: M9562
exact_source: GSE41978_3691_200_UP
source_species_code: MM
GEO_id: GSE41978
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in KLRG1 low [GeneID=10219] CD8 T effector cells during infection: wildtype versus BCL2L11 [GeneID=10018] knockout.

description_full:
[cell repeats an earlier one in this file: 1161 characters]


systematic_name: M9563
exact_source: GSE41978_3693_200_DN
source_species_code: MM
GEO_id: GSE41978
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in KLRG1 low [GeneID=10219] CD8 T effector cells during infection: ID2 [GeneID=10219] knockout versus BCL2L11 [GeneID=10018] knockout.

description_full:
[cell repeats an earlier one in this file: 1161 characters]


systematic_name: M9566
exact_source: GSE41978_3694_200_UP
source_species_code: MM
GEO_id: GSE41978
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in KLRG1 low [GeneID=10219] CD8 T effector cells during infection: ID2 and BCL2L11 [GeneID=3398;10018] versus BCL2L11 [GeneID=10018] knockout.

description_full:
[cell repeats an earlier one in this file: 1161 characters]


systematic_name: M9567
exact_source: GSE41978_3694_200_DN
source_species_code: MM
GEO_id: GSE41978
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in KLRG1 low [GeneID=10219] CD8 T effector cells during infection: ID2 and BCL2L11 [GeneID=3398;10018] versus BCL2L11 [GeneID=10018] knockout.

description_full:
[cell repeats an earlier one in this file: 1161 characters]


systematic_name: M9568
exact_source: GSE41978_3693_200_UP
source_species_code: MM
GEO_id: GSE41978
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in KLRG1 low [GeneID=10219] CD8 T effector cells during infection: ID2 [GeneID=10219] knockout versus BCL2L11 [GeneID=10018] knockout.

description_full:
[cell repeats an earlier one in this file: 1161 characters]


description_brief: Genes up-regulated in T reg from: peripheral lymph nodes versus thymic precursors.
systematic_name: M9569
exact_source: GSE42021_3779_200_UP
source_species_code: MM
GEO_id: GSE42021
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  We investigated at which stage of maturation commitment to a stable Foxp3-expressing phenotype takes place. We assessed stability of Foxp3 expression in thymic Foxp3+ Treg subsets of different maturity, defined by CD24 expression. Next we compared gene expression profiles of Foxp3+ Treg subsets (+) of different maturity (24lo, 24int, 24hi) and could identify a set of genes that were specifically up or downregulated in Foxp3+ Tregs, but not in Foxp3- conventional T cells, in a maturation-dependent manner.


systematic_name: M9584
exact_source: GSE42021_3787_200_UP
source_species_code: MM
GEO_id: GSE42021
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in thymic T reg: CD24 high [GeneID=100133941] versus CD24 int [GeneID=100133941].

description_full:
[cell repeats an earlier one in this file: 509 characters]


systematic_name: M9586
exact_source: GSE42021_3787_200_DN
source_species_code: MM
GEO_id: GSE42021
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in thymic T reg: CD24 high [GeneID=100133941] versus CD24 int [GeneID=100133941].

description_full:
[cell repeats an earlier one in this file: 509 characters]


systematic_name: M9587
exact_source: GSE42021_3788_200_UP
source_species_code: MM
GEO_id: GSE42021
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in thymic T reg: CD24 high [GeneID=100133941] versus CD24 low [GeneID=100133941].

description_full:
[cell repeats an earlier one in this file: 509 characters]


systematic_name: M9588
exact_source: GSE42021_3788_200_DN
source_species_code: MM
GEO_id: GSE42021
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in thymic T reg: CD24 high [GeneID=100133941] versus CD24 low [GeneID=100133941].

description_full:
[cell repeats an earlier one in this file: 509 characters]


systematic_name: M9590
exact_source: GSE42021_3789_200_DN
source_species_code: MM
GEO_id: GSE42021
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in thymic T reg: CD24 int [GeneID=100133941] versus CD24 low [GeneID=100133941].

description_full:
[cell repeats an earlier one in this file: 509 characters]


systematic_name: M9591
exact_source: GSE42021_3790_200_UP
source_species_code: MM
GEO_id: GSE42021
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in thymic T conv: CD24 high [GeneID=100133941] versus CD24 int [GeneID=100133941].

description_full:
[cell repeats an earlier one in this file: 509 characters]


systematic_name: M9593
exact_source: GSE42021_3790_200_DN
source_species_code: MM
GEO_id: GSE42021
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in thymic T conv: CD24 high [GeneID=100133941] versus CD24 int [GeneID=100133941].

description_full:
[cell repeats an earlier one in this file: 509 characters]


systematic_name: M9594
exact_source: GSE42021_3791_200_UP
source_species_code: MM
GEO_id: GSE42021
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in thymic T conv: CD24 high [GeneID=100133941] versus CD24 low [GeneID=100133941].

description_full:
[cell repeats an earlier one in this file: 509 characters]


systematic_name: M9595
exact_source: GSE42021_3791_200_DN
source_species_code: MM
GEO_id: GSE42021
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in thymic T conv: CD24 high [GeneID=100133941] versus CD24 low [GeneID=100133941].

description_full:
[cell repeats an earlier one in this file: 509 characters]


systematic_name: M9596
exact_source: GSE42021_3792_200_UP
source_species_code: MM
GEO_id: GSE42021
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in thymic T conv: CD24 int [GeneID=100133941] versus CD24 low [GeneID=100133941].

description_full:
[cell repeats an earlier one in this file: 509 characters]


systematic_name: M9597
exact_source: GSE42021_3792_200_DN
source_species_code: MM
GEO_id: GSE42021
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in thymic T conv: CD24 int [GeneID=100133941] versus CD24 low [GeneID=100133941].

description_full:
[cell repeats an earlier one in this file: 509 characters]


description_brief: Genes up-regulated in T reg: wildtype versus DNMT1 [GeneID=1786] knockout.
systematic_name: M9620
exact_source: GSE27434_3798_200_UP
source_species_code: MM
GEO_id: GSE27434
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  We investigated the role of DNMT1 in immune homeostasis by generating mice lacking DNMT1 in Foxp3+ T-regulatory (Treg) cells. These mice showed decreased peripheral Foxp3+ Tregs, complete loss of Foxp3+ Treg suppressive functions in vitro and in vivo, and died from autoimmunity by 3-4 weeks unless they received perinatal transfer of wild-type Tregs that prolonged their survival. Methylation of CpG-sites in the TSDR region of Foxp3 was unaffected by DNMT1 deletion, but microarray revealed more >500 proinflammatory and other genes were upregulated in DNMT1-/- Tregs. CD4-Cre-mediated DNMT1 deletion showed inability of conventional T cells to convert to Foxp3+ Treg under appropriate polarizing conditions. Hence, DNMT1 is absolutely necessary for maintenance of the gene program required for normal Treg development and function.


description_brief: Genes up-regulated in peripheral blood monocytes (PBMC): control versus IL10 [GeneID=3586].
systematic_name: M9622
exact_source: GSE43700_3701_200_UP
source_species_code: HS
GEO_id: GSE43700
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  The immune mechanisms that control resistance vs. susceptibility to mycobacterial infection in humans were investigated by studying leprosy skin lesions, the site where the battle between the host and the pathogen is joined. Using an integrative genomics approach, we found an inverse correlation between of IFN-beta and IFN-gamma gene expression programs at the site of disease. The Type II IFN, IFN-gamma and its downstream vitamin D-dependent antimicrobial genes were preferentially expressed in the lesions from patients with the self-healing tuberculoid form of the disease and mediated antimicrobial activity against the pathogen, Mycobacterium leprae in vitro. In contrast, the Type I IFN, IFN-beta and its downstream genes, including IL-27 and IL-10, were induced in monocytes by M. leprae in vitro, and were preferentially expressed in the lesions of disseminated and progressive lepromatous form. The IFN-gamma induced macrophage antimicrobial response was inhibited by IFN-beta/IL-10, by a mechanism involving blocking the generation of bioactive 1,25-dihyroxy vitamin D as well as inhibiting induction of antimicrobial peptides cathelicidin and DEFB4. The ability of IFN-B to inhibit the IFN-gamma induced vitamin D pathway including antimicrobial activity was reversed by neutralization of IL-10, suggesting a possible target for therapeutic intervention. Finally, a common IFN-beta and IL-10 gene signature was identified in both the skin lesions of leprosy patients and in the peripheral blood of active tuberculosis patients. Together these data suggest that the ability of IFN-beta to downregulate protective IFN-gamma responses provides one general mechanism by which some bacterial pathogens of humans evade protective host responses and contribute to pathogenesis.


description_brief: Genes up-regulated in CD4 [GeneID=920] T helper cells Th0: control versus NaCl treatment.
systematic_name: M9624
exact_source: GSE43957_2410_200_UP
source_species_code: MM
GEO_id: GSE43957
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  Th17 cells are highly proinflammatory cells that are critical for clearing extracellular pathogens like fungal infections and for induction of multiple autoimmune diseases1. IL-23 plays a critical role in stabilizing and endowing Th17 cells with pathogenic effector functions2. Previous studies have shown that IL-23 signaling reinforces the Th17 phenotype by increasing expression of IL-23 receptor (IL-23R)3. However, the precise molecular mechanism by which IL-23 sustains the Th17 response and induces pathogenic effector functions has not been elucidated. Here, we used unbiased transcriptional profiling of developing Th17 cells to construct a model of their signaling network and identify major nodes that regulate Th17 development. We identified serum glucocorticoid kinase-1 (SGK1), as an essential node downstream of IL-23 signaling, critical for regulating IL-23R expression and for stabilizing the Th17 cell phenotype by deactivation of Foxo1, a direct repressor of IL-23R expression. A serine-threonine kinase homologous to AKT4, SGK1 has been associated with cell cycle and apoptosis, and has been shown to govern Na+ transport and homeostasis5, 6 7, 8. We here show that a modest increase in salt (NaCl) concentration induces SGK1 expression, promotes IL-23R expression and enhances Th17 cell differentiation in vitro and in vivo, ultimately accelerating the development of autoimmunity. The loss of SGK1 resulted in abrogation of Na+-mediated Th17 differentiation in an IL-23-dependent manner. These data indicate that SGK1 is a critical regulator for the induction of pathogenic Th17 cells and provides a molecular insight by which an environmental factor such as a high salt diet could trigger Th17 development and promote tissue inflammation.


systematic_name: M9627
exact_source: GSE43956_2411_200_UP
source_species_code: MM
GEO_id: GSE43956
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T helper Th17 cells: wildtype versus SGK1 [GeneID-6446] knockout.

description_full:
  Th17 cells are highly proinflammatory cells that are critical for clearing extracellular pathogens like fungal infections and for induction of multiple autoimmune diseases1. IL-23 plays a critical role in stabilizing and endowing Th17 cells with pathogenic effector functions2. Previous studies have shown that IL-23 signaling reinforces the Th17 phenotype by increasing expression of IL-23 receptor (IL-23R)3. However, the precise molecular mechanism by which IL-23 sustains the Th17 response and induces pathogenic effector functions has not been elucidated. Here, we used unbiased transcriptional profiling of developing Th17 cells to construct a model of their signaling network and identify major nodes that regulate Th17 development. We identified serum glucocorticoid kinase-1 (SGK1), as an essential node downstream of IL-23 signaling, critical for regulating IL-23R expression and for stabilizing the Th17 cell phenotype by deactivation of Foxo1, a direct repressor of IL-23R expression. A serine-threonine kinase homologous to AKT4, SGK1 has been associated with cell cycle and apoptosis, and has been shown to govern Na+ transport and homeostasis5, 6 7, 8. We here show that a modest increase in salt (NaCl) concentration induces SGK1 expression, promotes IL-23R expression and enhances Th17 cell differentiation in vitro and in vivo, ultimately accelerating the development of autoimmunity. The loss of SGK1 resulted in abrogation of Na+-mediated Th17 differentiation in an IL-23-dependent manner. These data indicate that SGK1 is a critical regulator for the induction of pathogenic Th17 cells and provides a molecular insight by which an environmental factor such as a high salt diet could trigger Th17 development and promote tissue inflammation.


systematic_name: M9628
exact_source: GSE43956_2411_200_DN
source_species_code: MM
GEO_id: GSE43956
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T helper Th17 cells: wildtype versus SGK1 [GeneID-6446] knockout.

description_full:
[cell repeats an earlier one in this file: 1761 characters]


systematic_name: M9629
exact_source: GSE43955_2417_200_UP
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T helper cells (42h): Th0 versus TGFB1 and IL6 [GeneID=7040;3569].

description_full:
  Despite their enormous importance, the molecular circuits that control the differentiation of Th17 cells remain largely unknown. Recent studies have reconstructed regulatory networks in mammalian cells, but have focused on short-term responses and relied on perturbation approaches that cannot be applied to primary T cells. Here, we develop a systematic strategy – combining transcriptional profiling at high temporal resolution, novel computational algorithms, and innovative nanowire-based tools for performing gene perturbations in primary T cells – to derive and experimentally validate a temporal model of the dynamic regulatory network that controls Th17 differentiation. The network is arranged into two self-reinforcing and mutually antagonistic modules that either suppress or promote Th17 differentiation. The two modules contain 12 novel regulators with no previous implication in Th17 differentiation, which may be essential to maintain the appropriate balance of Th17 and other CD4+ T cell subsets. Overall, our study identifies and validates 39 regulatory factors that are embedded within a comprehensive temporal network and identifies novel drug targets and organizational principles for the differentiation of Th17 cells.


systematic_name: M9632
exact_source: GSE43955_2417_200_DN
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T helper cells (42h): Th0 versus TGFB1 and IL6 [GeneID=7040;3569].

description_full:
  Despite their enormous importance, the molecular circuits that control the differentiation of Th17 cells remain largely unknown. Recent studies have reconstructed regulatory networks in mammalian cells, but have focused on short-term responses and relied on perturbation approaches that cannot be applied to primary T cells. Here, we develop a systematic strategy – combining transcriptional profiling at high temporal resolution, novel computational algorithms, and innovative nanowire-based tools for performing gene perturbations in primary T cells – to derive and experimentally validate a temporal model of the dynamic regulatory network that controls Th17 differentiation. The network is arranged into two self-reinforcing and mutually antagonistic modules that either suppress or promote Th17 differentiation. The two modules contain 12 novel regulators with no previous implication in Th17 differentiation, which may be essential to maintain the appropriate balance of Th17 and other CD4+ T cell subsets. Overall, our study identifies and validates 39 regulatory factors that are embedded within a comprehensive temporal network and identifies novel drug targets and organizational principles for the differentiation of Th17 cells.


systematic_name: M9633
exact_source: GSE43955_2418_200_UP
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T helper cells (52h): Th0 versus TGFB1 and IL6 [GeneID=7040;3569].

description_full:
  Despite their enormous importance, the molecular circuits that control the differentiation of Th17 cells remain largely unknown. Recent studies have reconstructed regulatory networks in mammalian cells, but have focused on short-term responses and relied on perturbation approaches that cannot be applied to primary T cells. Here, we develop a systematic strategy – combining transcriptional profiling at high temporal resolution, novel computational algorithms, and innovative nanowire-based tools for performing gene perturbations in primary T cells – to derive and experimentally validate a temporal model of the dynamic regulatory network that controls Th17 differentiation. The network is arranged into two self-reinforcing and mutually antagonistic modules that either suppress or promote Th17 differentiation. The two modules contain 12 novel regulators with no previous implication in Th17 differentiation, which may be essential to maintain the appropriate balance of Th17 and other CD4+ T cell subsets. Overall, our study identifies and validates 39 regulatory factors that are embedded within a comprehensive temporal network and identifies novel drug targets and organizational principles for the differentiation of Th17 cells.


systematic_name: M9635
exact_source: GSE43955_2412_200_UP
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T helper cells (1h): Th0 versus TGFB1 and IL6 [GeneID=7040;3569].

description_full:
[cell repeats an earlier one in this file: 1239 characters]


systematic_name: M9637
exact_source: GSE43955_2412_200_DN
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T helper cells (1h): Th0 versus TGFB1 and IL6 [GeneID=7040;3569].

description_full:
[cell repeats an earlier one in this file: 1239 characters]


systematic_name: M9640
exact_source: GSE43955_2413_200_UP
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T helper cells (4h): Th0 versus TGFB1 and IL6 [GeneID=7040;3569].

description_full:
[cell repeats an earlier one in this file: 1239 characters]


systematic_name: M9641
exact_source: GSE43955_2413_200_DN
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T helper cells (4h): Th0 versus TGFB1 and IL6 [GeneID=7040;3569].

description_full:
[cell repeats an earlier one in this file: 1239 characters]


systematic_name: M9643
exact_source: GSE43955_2414_200_UP
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T helper cells (10h): Th0 versus TGFB1 and IL6 [GeneID=7040;3569].

description_full:
[cell repeats an earlier one in this file: 1239 characters]


systematic_name: M9644
exact_source: GSE43955_2414_200_DN
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T helper cells (10h): Th0 versus TGFB1 and IL6 [GeneID=7040;3569].

description_full:
[cell repeats an earlier one in this file: 1239 characters]


systematic_name: M9646
exact_source: GSE43955_2415_200_UP
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T helper cells (20h): Th0 versus TGFB1 and IL6 [GeneID=7040;3569].

description_full:
[cell repeats an earlier one in this file: 1239 characters]


systematic_name: M9647
exact_source: GSE43955_2415_200_DN
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T helper cells (20h): Th0 versus TGFB1 and IL6 [GeneID=7040;3569].

description_full:
[cell repeats an earlier one in this file: 1239 characters]


systematic_name: M9649
exact_source: GSE43955_2416_200_UP
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T helper cells (30h): Th0 versus TGFB1 and IL6 [GeneID=7040;3569].

description_full:
[cell repeats an earlier one in this file: 1239 characters]


systematic_name: M9650
exact_source: GSE43955_2416_200_DN
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T helper cells (30h): Th0 versus TGFB1 and IL6 [GeneID=7040;3569].

description_full:
[cell repeats an earlier one in this file: 1239 characters]


systematic_name: M9652
exact_source: GSE43955_2424_200_UP
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T helper cells (52h): Th0 versus Th17 treated with TGFB1, IL6 [GeneID=7040;3569] and IL-23.

description_full:
[cell repeats an earlier one in this file: 1239 characters]


systematic_name: M9653
exact_source: GSE43955_2424_200_DN
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T helper cells (52h): Th0 versus Th17 treated with TGFB1, IL6 [GeneID=7040;3569] and IL-23.

description_full:
[cell repeats an earlier one in this file: 1239 characters]


systematic_name: M9654
exact_source: GSE43955_2418_200_DN
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T helper cells (52h): Th0 versus TGFB1 and IL6 [GeneID=7040;3569].

description_full:
[cell repeats an earlier one in this file: 1239 characters]


systematic_name: M9655
exact_source: GSE43955_2419_200_UP
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T helper cells (60h): Th0 versus TGFB1 and IL6 [GeneID=7040;3569].

description_full:
[cell repeats an earlier one in this file: 1239 characters]


systematic_name: M9657
exact_source: GSE43955_2419_200_DN
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T helper cells (60h): Th0 versus TGFB1 and IL6 [GeneID=7040;3569].

description_full:
[cell repeats an earlier one in this file: 1239 characters]


systematic_name: M9667
exact_source: GSE43955_2430_200_UP
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T helper cells Th17 (52h): TGFB1 and IL6 [GeneID=7040;3569] versus TGFB1, IL6 [GeneID=7040;3569] and IL-23.

description_full:
[cell repeats an earlier one in this file: 1239 characters]


systematic_name: M9668
exact_source: GSE43955_2430_200_DN
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T helper cells Th17 (52h): TGFB1 and IL6 [GeneID=7040;3569] versus TGFB1, IL6 [GeneID=7040;3569] and IL-23.

description_full:
[cell repeats an earlier one in this file: 1239 characters]


systematic_name: M9671
exact_source: GSE43955_2431_200_UP
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T helper cells Th17 (60h): TGFB1 and IL6 [GeneID=7040;3569] versus TGFB1, IL6 [GeneID=7040;3569] and IL-23.

description_full:
[cell repeats an earlier one in this file: 1239 characters]


systematic_name: M9672
exact_source: GSE43955_2431_200_DN
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T helper cells Th17 (60h): TGFB1 and IL6 [GeneID=7040;3569] versus TGFB1, IL6 [GeneID=7040;3569] and IL-23.

description_full:
[cell repeats an earlier one in this file: 1239 characters]


systematic_name: M9674
exact_source: GSE43955_2432_200_UP
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T helper cells Th17 treated with TGFB1 and IL6 [GeneID=7040;3569]: 1h versus 10h.

description_full:
[cell repeats an earlier one in this file: 1239 characters]


systematic_name: M9675
exact_source: GSE43955_2432_200_DN
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T helper cells Th17 treated with TGFB1 and IL6 [GeneID=7040;3569]: 1h versus 10h.

description_full:
[cell repeats an earlier one in this file: 1239 characters]


systematic_name: M9676
exact_source: GSE43955_2433_200_UP
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T helper cells Th17 treated with TGFB1 and IL6 [GeneID=7040;3569]: 1h versus 20h.

description_full:
[cell repeats an earlier one in this file: 1239 characters]


systematic_name: M9677
exact_source: GSE43955_2433_200_DN
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T helper cells Th17 treated with TGFB1 and IL6 [GeneID=7040;3569]: 1h versus 20h.

description_full:
[cell repeats an earlier one in this file: 1239 characters]


systematic_name: M9679
exact_source: GSE43955_2434_200_UP
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T helper cells Th17 treated with TGFB1 and IL6 [GeneID=7040;3569]: 1h versus 42h.

description_full:
[cell repeats an earlier one in this file: 1239 characters]


systematic_name: M9680
exact_source: GSE43955_2434_200_DN
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T helper cells Th17 treated with TGFB1 and IL6 [GeneID=7040;3569]: 1h versus 42h.

description_full:
[cell repeats an earlier one in this file: 1239 characters]


systematic_name: M9682
exact_source: GSE43955_2435_200_UP
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T helper cells Th17 treated with TGFB1 and IL6 [GeneID=7040;3569]: 1h versus 60h.

description_full:
[cell repeats an earlier one in this file: 1239 characters]


systematic_name: M9685
exact_source: GSE43955_2435_200_DN
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T helper cells Th17 treated with TGFB1 and IL6 [GeneID=7040;3569]: 1h versus 60h.

description_full:
[cell repeats an earlier one in this file: 1239 characters]


systematic_name: M9686
exact_source: GSE43955_2429_200_UP
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T helper cells Th17 treated with TGFB1 and IL6 [GeneID=7040;3569]: 10h versus 60h.

description_full:
[cell repeats an earlier one in this file: 1239 characters]


systematic_name: M9687
exact_source: GSE43955_2429_200_DN
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T helper cells Th17 treated with TGFB1 and IL6 [GeneID=7040;3569]: 10h versus 60h.

description_full:
[cell repeats an earlier one in this file: 1239 characters]


systematic_name: M9688
exact_source: GSE43955_2425_200_DN
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T helper cells (60h): Th0 versus Th17 treated with TGFB1, IL6 [GeneID=7040;3569] and IL-23.

description_full:
[cell repeats an earlier one in this file: 1239 characters]


systematic_name: M9691
exact_source: GSE43955_2425_200_UP
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T helper cells (60h): Th0 versus Th17 treated with TGFB1, IL6 [GeneID=7040;3569] and IL-23.

description_full:
[cell repeats an earlier one in this file: 1239 characters]


systematic_name: M9696
exact_source: GSE43955_2428_200_UP
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in CD4 [GeneID=920] T helper cells Th17 treated with TGFB1 and IL6 [GeneID=7040;3569]: 10h versus 30h.

description_full:
[cell repeats an earlier one in this file: 1239 characters]


systematic_name: M9697
exact_source: GSE43955_2428_200_DN
source_species_code: MM
GEO_id: GSE43955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in CD4 [GeneID=920] T helper cells Th17 treated with TGFB1 and IL6 [GeneID=7040;3569]: 10h versus 30h.

description_full:
[cell repeats an earlier one in this file: 1239 characters]


description_brief: Genes up-regulated in immature dendritic cells: untreated versus IL27 [GeneID=246778].
systematic_name: M9699
exact_source: GSE44732_3800_200_UP
source_species_code: HS
GEO_id: GSE44732
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  IL-27 treated DCs were shown to be highly potent inhibitors of cis HIV-1, particularly of CCR5 tropic strains. Microarray studies of IL-27 treated DCs showed no up-regulation of Type I (IFN) gene expression. Neutralization of the Type-I IFN receptor had no impact on the HIV inhibition. Lastly, IL-27 mediated inhibition was shown to act post-viral entry and prior to completion of reverse transcription. These results show for the first time that IL-27 is a potent inhibitor of cis HIV-1 infection in DCs by a Type I IFN independent mechanism.


systematic_name: M9701
exact_source: GSE44955_3901_200_DN
source_species_code: HS
GEO_id: GSE44955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes down-regulated in macrophage differentiated by: CSF1 [GeneID=1435] versus CSF1 [GeneID=1435] and IL27 [GeneID=246778].

description_full:
  In this study, we hypothesized that IL-27 could induce the expression of novel miRNAs in macrophages which may have functional relevance in terms of anti-viral activity. In this study, primary monocytes were differentiated into macrophages using M-CSF (M-Mac) or with a combination of M-CSF and IL-27 (I-Mac) for seven days. Following this, total RNA was extracted from these cells and deep sequencing was performed, in parallel with gene expression microarrays. Using the novel miRNA discovery software, miRDeep, seven novel miRNAs were discovered in the macrophages, four of which were expressed higher in I-Mac (miRNAs 2.1, 8.1, 9.1 and 14.2) whilst three were detected in both M-Mac and I-Mac (miRNAs 9.3, 13.6 and 15.8). The expression of six of the seven novel miRNAs was highly correlated with qRT-PCR using specific primer/probes designed for the novel miRNAs. Gene expression microarray further demonstrated that a number of genes were potentially targeted by these differentially expressed novel miRNAs.


systematic_name: M9704
exact_source: GSE44955_3901_200_UP
source_species_code: HS
GEO_id: GSE44955
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in macrophage differentiated by: CSF1 [GeneID=1435] versus CSF1 [GeneID=1435] and IL27 [GeneID=246778].

description_full:
  In this study, we hypothesized that IL-27 could induce the expression of novel miRNAs in macrophages which may have functional relevance in terms of anti-viral activity. In this study, primary monocytes were differentiated into macrophages using M-CSF (M-Mac) or with a combination of M-CSF and IL-27 (I-Mac) for seven days. Following this, total RNA was extracted from these cells and deep sequencing was performed, in parallel with gene expression microarrays. Using the novel miRNA discovery software, miRDeep, seven novel miRNAs were discovered in the macrophages, four of which were expressed higher in I-Mac (miRNAs 2.1, 8.1, 9.1 and 14.2) whilst three were detected in both M-Mac and I-Mac (miRNAs 9.3, 13.6 and 15.8). The expression of six of the seven novel miRNAs was highly correlated with qRT-PCR using specific primer/probes designed for the novel miRNAs. Gene expression microarray further demonstrated that a number of genes were potentially targeted by these differentially expressed novel miRNAs.


description_brief: Genes up-regulated in CD4 [GeneID=920] Th1 cells: wildtype versus EGR2 [GeneID=1959] knockout.
systematic_name: M9705
exact_source: GSE46242_3745_200_UP
source_species_code: MM
GEO_id: GSE46242
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_full:
  T cell anergy is one of the mechanisms contributing to peripheral tolerance, particularly in the context of progressively growing tumors and in tolerogenic treatments promoting allograft acceptance. We recently reported that early growth response gene 2 (Egr2) is a critical transcription factor for the induction of anergy in vitro and in vivo, which was identified based on its ability to regulate the expression of inhibitory signaling molecules diacylglycerol kinase (DGK)-a and -z. We reasoned that other transcriptional targets of Egr2 might encode additional factors important for T cell anergy and immune regulation. Thus, we conducted two sets of genome-wide screens: gene expression profiling of wild type versus Egr2-deleted T cells treated under anergizing conditions, and a ChIP-Seq analysis to identify genes that bind Egr2 in anergic cells. Merging of these data sets revealed 49 targets that are directly regulated by Egr2. Among these are inhibitory signaling molecules previously reported to contribute to T cell anergy, but unexpectedly, also cell surface molecules and secreted factors, including lymphocyte-activation gene 3 (Lag3), Class-I-MHC-restricted T cell associated molecule (Crtam), Semaphorin 7A (Sema7A), and chemokine CCL1. These observations suggest that anergic T cells might not simply be functionally inert, and may have additional functional properties oriented towards other cellular components of the immune system.


systematic_name: M9707
exact_source: GSE46242_3746_200_UP
source_species_code: MM
GEO_id: GSE46242
contributor: Jernej Godec
contrib_organization: Dana-Farber Cancer Institute
description_brief:
  Genes up-regulated in anergic CD4 [GeneID=920] Th1 cells: wildtype versus EGR2 [GeneID=1959] knockout.

description_full:
  T cell anergy is one of the mechanisms contributing to peripheral tolerance, particularly in the context of progressively growing tumors and in tolerogenic treatments promoting allograft acceptance. We recently reported that early growth response gene 2 (Egr2) is a critical transcription factor for the induction of anergy in vitro and in vivo, which was identified based on its ability to regulate the expression of inhibitory signaling molecules diacylglycerol kinase (DGK)-a and -z. We reasoned that other transcriptional targets of Egr2 might encode additional factors important for T cell anergy and immune regulation. Thus, we conducted two sets of genome-wide screens: gene expression profiling of wild type versus Egr2-deleted T cells treated under anergizing conditions, and a ChIP-Seq analysis to identify genes that bind Egr2 in anergic cells. Merging of these data sets revealed 49 targets that are directly regulated by Egr2. Among these are inhibitory signaling molecules previously reported to contribute to T cell anergy, but unexpectedly, also cell surface molecules and secreted factors, including lymphocyte-activation gene 3 (Lag3), Class-I-MHC-restricted T cell associated molecule (Crtam), Semaphorin 7A (Sema7A), and chemokine CCL1. These observations suggest that anergic T cells might not simply be functionally inert, and may have additional functional properties oriented towards other cellular components of the immune system.


