Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Id2 acts as a metabolic checkpoint underpinning Th17 cell fate decision [scRNA-seq]

ABSTRACT: T helper 17 (Th17) cells protect barrier tissues but also trigger autoimmunity. The precise mechanisms control these opposing processes remain unclear. We identify Id2 as a key factor for pathogenic Th17 cells. Id2 expression is markedly elevated in Myelin-reactive T cells from multiple sclerosis (MS) patients and autoimmune mice. Mice lacking Id2 in Th17 cells completely fail to develop neuroinflammation and do not generate neuron-pathogenic Th17 subset.

ORGANISM(S): Mus musculus

PROVIDER: GSE295290 | GEO | 2025/07/13

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Id2 acts as a metabolic checkpoint underpinning Th17 cell fate decision [RNA-seq]

Project description:T helper 17 (Th17) cells protect barrier tissues but also trigger autoimmunity. The precise mechanisms control these opposing processes remain unclear. We identify Id2 as a key factor for pathogenic Th17 cells. Id2 expression is markedly elevated in Myelin-reactive T cells from multiple sclerosis (MS) patients and autoimmune mice. Mice lacking Id2 in Th17 cells completely fail to develop neuroinflammation and do not generate neuron-pathogenic Th17 subset.

2025-07-13 | GSE295288 | GEO

Id2 acts as a metabolic checkpoint underpinning Th17 cell fate decision [CUT&Tag]

2025-07-13 | GSE295289 | GEO

Transcription factor EGR2 controls homing and pathogenicity of TH17 cells in the central nervous system.

Project description:CD4+ T helper 17 (TH17) cells protect barrier tissues but also trigger autoimmunity. The mechanisms behind these opposing processes remain unclear. Here, we found that the transcription factor EGR2 controlled the transcriptional program of pathogenic TH17 cells in the central nervous system (CNS) but not that of protective TH17 cells at barrier sites. EGR2 was significantly elevated in myelin-reactive CD4+ T cells from patients with multiple sclerosis and mice with autoimmune neuroinflammation. The EGR2 transcriptional program was intricately woven within the TH17 cell transcriptional regulatory network and showed high interconnectivity with core TH17 cell-specific transcription factors. Mechanistically, EGR2 enhanced TH17 cell differentiation and myeloid cell recruitment to the CNS by upregulating pathogenesis-associated genes and myelomonocytic chemokines. T cell-specific deletion of Egr2 attenuated neuroinflammation without compromising the host’s ability to control infections. Our study shows that EGR2 regulates tissue-specific and disease-specific functions in pathogenic TH17 cells in the CNS.

2021-05-19 | GSE168288 | GEO

Transcription factor EGR2 controls homing and pathogenicity of TH17 cells in the central nervous system.

2023-06-28 | GSE226795 | GEO

Transcription factor EGR2 controls homing and pathogenicity of TH17 cells in the central nervous system.

2023-06-28 | GSE224960 | GEO

Mouse Th17 T cells, IL-23 stimulated

Project description:Interleukin 23 (IL-23) triggers pathogenic features in pro-inflammatory, IL-17-secreting T cells (Th17 and Tγδ17) that play a key role in the development of inflammatory diseases. However, the IL-23 signaling cascade remains largely undefined. Here we used quantitative phosphoproteomics to characterize IL-23 signaling in primary murine Th17 cells. We quantified 6,888 phosphorylation sites in Th17 cells, and found 168 phosphorylations regulated upom IL-23 stimulation. IL-23 increased the phosphorylation of the myosin regulatory light chain (RLC), an actomyosin contractibility marker, in Th17 and Tγδ cells. IL-23-induced RLC phosphorylation required JAK2 and ROCK catalytic activity, and the study of the IL-23/ROCK axis revealed an unexpected role of IL-23 in the migration of Tγδ17 and Th17 cells. Moreover, pharmacological inhibition of ROCK reduced Tγδ17 recruitment to inflamed skin upon challenge with inflammatory agent Imiquimod. This work: i) provides new insights into phosphorylation networks that control Th17 cells, ii) widely expands the current knowledge on IL-23 signaling, and iii) contributes to the increasing list of immune cells subsets characterized by global phosphoproteomic approaches.

2020-03-25 | PXD016633 | Pride

Transcription factor TCF1 binds Rorgt and orchestrates a regulatory network that determines homeostatic Th17 cell state [RNA-seq]

Project description:CD4+ T helper 17 (Th17) cells encompass a spectrum of cell states including homeostatic cells that maintain physiological functions such as barrier integrity and pathogenic cells that drive autoimmune tissue inflammation. Identifying the regulators that determine these cell states will provide means to control tissue inflammation without compromising the physiological functions of Th17 cells. Here, we identified TCF1 as the key regulator that determines Th17 cell state. IL-23, a cytokine critical for inducing pathogenic Th17 cells, decreased TCF1 expression. Consistent with this observation, conditional deletion of Tcf7/TCF1 in mature myelin-specific T cells conferred pathogenicity to homeostatic Th17 cells independent of IL-23. Conversely, sustained TCF1 expression impaired acquisition of pathogenicity. Integration of transcriptional and chromatin accessibility data showed that TCF1 maintained homeostatic state through a regulatory network involving ETS family transcription factors, EGR1, and FOXO1 and by binding to and interfering with RORt activity. Our findings provide mechanistic insight into how the homeostatic and pathogenic Th17 cell states are determined and into the association of genetic variants in TCF7 with susceptibility to autoimmunity.

2024-11-03 | GSE233907 | GEO

Transcription factor TCF1 binds Rorgt and orchestrates a regulatory network that determines homeostatic Th17 cell state [ATAC-seq]

2024-11-03 | GSE233905 | GEO

Transcriptional signature of human pro-inflammatory TH17 cells [TH17 clones]

Project description:Human IL-10– and IL-10+ TH17 clones maintained their pro- or anti-inflammatory characteristics after long-term culture. There were similarities between human IL-10– vs. IL-10+ TH17 clones and mouse pathogenic vs. non-pathogenic TH17 cells.

2017-09-29 | GSE104023 | GEO

Induction and molecular signature of pathogenic Th17 cells

Project description:TGF-beta3 produced by developing Th17 cells induces highly pathogenic T cells that are functionally and molecularly distinct from TGF-beta1-induced Th17 cells. The microarray data represent a distinct molecular signature for pathogenic versus non-pathogenic Th17 cells.

2012-09-01 | GSE39820 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data