Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cholinergic control of Th17 cell pathogenicity in experimental autoimmune encephalomyelitis [ATAC-seq]

ABSTRACT: Elucidate open chromatin regions associated with ChAT-GFP expression in in vitro polarized Th17 cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE215671 | GEO | 2022/11/13

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Cholinergic control of Th17 cell pathogenicity in experimental autoimmune encephalomyelitis [RNA-seq]

Project description:Elucidate a ChAT-associated gene expression program shared in ChAT-GFP-expressing splenic lymphocytes. (Seeking to answer the question, "Can we find a transcription factor that drives ChAT expression in lymphocytes?")

2022-11-13 | GSE215672 | GEO

Cholinergic control of Th17 cell pathogenicity in experimental autoimmune encephalomyelitis

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-11-13 | GSE215673 | GEO

Integrin α3-dependent gene expression in Th17 cells generated during experimental autoimmune encephalomyelitis

Project description:To understand the global gene expression changes in Itga3-deficient Th17 cells, we performed RNA-seq with fate-mapped Th17 cells isolated from inguinal lymph nodes of EAE-induced mice at day 7 post EAE induction.

2023-09-27 | GSE214418 | GEO

Gene expression data from polarized T helper cells isolated from mice with opticospinal (OSE) experimental autoimmune encephalomyelitis (EAE)

Project description:T cells from the spleen of a mixed-gender pool of four double-transgenic 2D2 (TCRMOG) x IgHMOG mice (OSE) mice, which spontaneously develop experimental autoimmune encephalomyelitis (EAE), were used to derive TH1- and TH17-polarized cells, as described in https://doi.org/10.1371/journal.pone.0015531. Here, expression was compared, first, between TH1 and naïve TH0 and, second, between TH17 and naïve TH0 cells.

2020-08-21 | E-MTAB-9133 | biostudies-arrayexpress

Human Th17 Cell differentiation

Project description:The early stages of human Th17 Cell differentiation were studied using label free proteomics to compare Th17 polarized CD4+ human T cells at 24 h and 72 h with activated cells (72 and 24 h) and Thp cells.

2019-01-28 | PXD008973 | Pride

Activin-A limits Th17 pathogenicity and autoimmune neuroinflammation via CD39 and CD73 ectonucleotidases and Hif1-α -dependent pathways

Project description:In multiple sclerosis (MS), Th17 cells are critical drivers of autoimmune central nervous system (CNS) inflammation and demyelination. Th17 cells exhibit functional heterogeneity fostering both pathogenic and non-pathogenic, tissue-protective functions. Still, the factors that control Th17 pathogenicity remain incompletely defined. Here, using experimental autoimmune encephalomyelitis (EAE), an established mouse MS model, we report that therapeutic administration of activin-A ameliorates disease severity and alleviates CNS immunopathology and demyelination, associated with decreased activation of Th17 cells. In fact, activin-A signaling through activin-like kinase (ALK)4 receptor represses pathogenic transcriptional programs in Th17-polarized cells, while it enhances anti-inflammatory gene modules. Whole genome profiling and in vivo functional studies revealed that activation of the ATP-depleting CD39 and CD73 ectonucleotidases is essential for activin-A-induced suppression of the pathogenic signature and the encephalitogenic functions of Th17 cells. Mechanistically, aryl hydrocarbon receptor, along with STAT3 and c-Maf, are recruited to promoter elements on Entpd1 and Nt5e (encoding CD39 and CD73, respectively) and other anti-inflammatory genes, and control their expression in Th17 cells in response to activin-A. Notably, we show that activin-A negatively regulates the metabolic sensor, hypoxia-inducible factor-1 and key inflammatory proteins linked to pathogenic Th17 cell states. Of translational relevance, we demonstrate that activin-A is induced in the CNS of individuals with MS and restrains human Th17 cell responses. These findings uncover activin-A as a novel critical controller of Th17 cell pathogenicity that can be targeted for the suppression of autoimmune CNS inflammation.

2020-03-06 | GSE146439 | GEO

MicroRNA-21 promotes Th17 differentiation and mediates experimental autoimmune encephalomyelitis.

Project description: Not available

| S-EPMC4362225 | biostudies-literature

RGC-32 Promotes Th17 Cell Differentiation and Enhances Experimental Autoimmune Encephalomyelitis.

Project description: Not available

| S-EPMC6197070 | biostudies-literature

Synthetic retinoid AM80 inhibits Th17 cells and ameliorates experimental autoimmune encephalomyelitis.

Project description: Not available

| S-EPMC2684188 | biostudies-literature

Prostaglandin I2 signaling drives Th17 differentiation and exacerbates experimental autoimmune encephalomyelitis.

Project description: Not available