GEO DataSets

(Submitter supplied) To understand molecular mechanisms by which JunB regulates Th17 differentiation, we performed ChIP-seq analyses of JunB-deficient and control Th17 cells.

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL21103

8 Samples

Download data: BED

(Submitter supplied) To understand molecular mechanisms by which JunB regulates Th17 differentiation, we performed microarray analyses of JunB-deficient and control Th17 cells.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

12 Samples

Download data: CEL

(Submitter supplied) Interleukin (IL)-17-producing T helper (Th17) cells are crucial for host defense against extracellular microbes and pathogenesis of autoimmune diseases. Here we show that the AP-1 transcription factor JunB is required for Th17 cell development. Junb-deficient CD4+ T cells are able to develop in vitro into various helper T subsets except Th17. The RNA-seq transcriptome analysis reveals that JunB is crucial for the Th17-specific gene expression program. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL17021

8 Samples

Download data: TXT

(Submitter supplied) The aim of this study was to identify differential gene expression resulting from the inhibition of RORgt in human CD4+ T cells.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL6244

20 Samples

Download data: CEL

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL21103 GPL13112

14 Samples

Download data: XLS

(Submitter supplied) Here we identify the activator protein-1 (AP-1) factor JunB as an essential regulator of Th17 cell identity. JunB activates the expression of Th17 lineage-specifying genes, and coordinately represses genes controlling Th1 and Treg fate. Through regulatory analysis, we find that JunB is a core regulator of global transcriptional programs that promote Th17 cell identity and restrict alternative CD4+ T cell potential.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

4 Samples

Download data: TAB

(Submitter supplied) Here we identify the activator protein-1 (AP-1) factor JunB as an essential regulator of Th17 cell identity. JunB activates the expression of Th17 lineage-specifying genes, and coordinately represses genes controlling Th1 and Treg fate. Through regulatory analysis, we find that JunB is a core regulator of global transcriptional programs that promote Th17 cell identity and restrict alternative CD4+ T cell potential.

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL21103 GPL13112

10 Samples

Download data: XLS

(Submitter supplied) T helper 17 (Th17) cells produce interleukin-17 (IL-17) cytokines and drive inflammatory responses in autoimmune diseases such as multiple sclerosis and rheumatoid arthritis. The differentiation of Th17 cells is dependent on the retinoic acid receptor-related orphan nuclear receptor RORgt. Here we identify REV-ERBa (encoded by Nr1d1), a member of the nuclear hormone receptor family (NHR), as a transcriptional repressor that antagonizes RORgt function in Th17 cells. more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL17021

2 Samples

Download data: BEDGRAPH, TXT

(Submitter supplied) Cell fate decision is mediated by epigenetic mechanisms. We have analyzed naive T cell differentiation into Th17 cells, which is regulated by environmental cytokines and their downstream transcription factors. RORγt is a lineage-specific master transcription factor for Th17 cells. Although epigenetic mechanisms have been implicated in Th17 cell differentiation, how transcription factors interact to activate epigenetic program is unclear. more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL13112

8 Samples

Download data: WIG

(Submitter supplied) Cell fate decision is mediated by epigenetic mechanisms. We have analyzed naive T cell differentiation into Th17 cells, which is regulated by environmental cytokines and their downstream transcription factors. RORγt is a lineage-specific master transcription factor for Th17 cells. Although epigenetic mechanisms have been implicated in Th17 cell differentiation, how transcription factors interact to activate epigenetic program is unclear. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL17021

8 Samples

Download data: TDF, TXT, WIG

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Mus musculus; synthetic construct

Type:

Expression profiling by array; Non-coding RNA profiling by array

Platforms:

GPL16570 GPL16384

20 Samples

Download data: CEL, XLSX

(Submitter supplied) Combined analysis of mRNA and miRNA transcriptoms revealed a complex network regulating major immune regulatory signaling pathways

Organism:

Mus musculus; synthetic construct

Type:

Non-coding RNA profiling by array

Platform:

GPL16384

10 Samples

Download data: CEL

(Submitter supplied) Combined analysis of mRNA and miRNA transcriptoms revealed a complex network regulating major immune regulatory signaling pathways

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL16570

10 Samples

Download data: CEL

(Submitter supplied) STAT3 has a more profound effect on chromatin accessibility regulation than RORgt during Th17 cell differentiation.

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL21273

4 Samples

Download data: BW

(Submitter supplied) CD4+ T cells that selectively produce interleukin (IL)-17, are critical for host defense and autoimmunity. Crucial for T helper17 (Th17) cells in vivo, IL-23 has been thought to be incapable of driving initial differentiation. Rather, IL-6 and transforming growth factor (TGF)-β1 have been argued to be the factors responsible for initiating specification. Herein, we show that Th17 differentiation occurs in the absence of TGF-β signaling. more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL9185

3 Samples

Download data: BED, BEDGRAPH

(Submitter supplied) CD4+ T cells that selectively produce interleukin (IL)-17, are critical for host defense and autoimmunity1-4. Crucial for T helper17 (Th17) cells in vivo5,6, IL-23 has been thought to be incapable of driving initial differentiation. Rather, IL-6 and transforming growth factor (TGF)-β1 have been argued to be the factors responsible for initiating specification7-10. Herein, we show that Th17 differentiation occurs in the absence of TGF-β signaling. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

10 Samples

Download data: CEL

(Submitter supplied) RORγt is well recognized as the lineage defining transcription factor for TH17 cell development. However, the cell-intrinsic mechanisms that negatively regulate TH17 cell development and autoimmunity remain poorly understood. Here we demonstrate that the transcriptional repressor REV-ERBa is exclusively expressed in TH17 cells, competes with RORγt for their shared DNA consensus sequence, and negatively regulates TH17 cell development via repression of genes traditionally characterized as RORγt-dependent, including Il17a. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL19057

10 Samples

Download data: XLSX

(Submitter supplied) The project was designed to figure out the role of microglia in brain inflammation (EAE model). The first step was to find genes/pathways that are upregulated in the microglia during EAE progress but absent in the infiltrating monocytes. These genes/pathways may provide clues for studying the unique function of microglia in the brain inflammation that is disctinct from the infiltrating monocytes.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL17021

13 Samples

Download data: TXT

(Submitter supplied) We report that the Serum Amyloid A protein, SAA1, is a novel, soluble co-factor able to promote pathogenic TH17 differentiation.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24247

27 Samples

Download data: TXT

(Submitter supplied) Disruption of Ski/Smad4 license Th17 differentiation. TGF-b-Ski-Smad4-RORgt-Th17 axis

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL19057

8 Samples

Download data: BED