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

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

PROVIDER: PRJNA1254127 | ENA |

REPOSITORIES: ENA

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

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

| PRJNA1254140 | ENA

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

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

| PRJNA1254128 | ENA

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

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 | GSE295289 | GEO

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

2025-07-13 | GSE295288 | GEO

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

2025-07-13 | GSE295290 | GEO

Whole genome mRNA analysis of wild-type and Id2-deficient virus-specific CD8+ T cells after influenza infection

2013-05-03 | GSE44141 | GEO

Expression data from Id2-GFP- CDPs, Id2-GFP+ CDPs, Id2-GFP- pre-CD8, and Id2-GFP+ pre-CD8.

Project description:Expression data from Id2-GFP- CDPs, Id2-GFP+ CDPs, Id2-GFP- pre-CD8, and Id2-GFP+ pre-CD8.

| PRJNA509888 | ENA

Whole genome mRNA analysis of wild-type and Id2-deficient virus-specific CD8+ T cells after influenza infection

Project description:The transcription factor Inhibitor of DNA binding 2 (Id2) modulates T cell fate decisions but the molecular mechanism underpinning this regulation is unclear. Here, using whole genome mRNA analysis we show that loss of Id2 programs CD8+ T cells to adopt a memory fate with increased Eomesodermin and Tcf7 expression. Our findings reveal that the Id2-E2A axis orchestrates T cell differentiation through the induction or repression of downstream transcription factors essential for effector and memory T cell differentiation. Wild-type and Id2fl/flLckCre+ DbNP366-specific CD8+ T cells were isolated from the spleen of PR8-primed/HKx31-infected Ly5.2+Id2fl/flLckCre+:Ly5.1+ mixed bone marrow chimeric mice ten days after intranasal influenza infection and analysed by whole genome mRNA analysis. Three biological replicates of each genotype were subjected to microarray analysis.

2013-05-03 | E-GEOD-44141 | biostudies-arrayexpress

ID2 controls differentiation of entero-endocrine cells in mouse small intestine

Project description:Aim: The mammalian gut is the largest endocrine organ. Dozens of hormones secreted by enteroendocrine cells regulate a variety of physiological functions of the gut but also of the pancreas and brain. Here, we examined the role of the helix-loop-helix transcription factor ID2 during the differentiation of intestinal stem cells along the enteroendocrine lineage. Methods: To assess the functions of ID2 in the adult mouse small intestine, we used single-cell RNA sequencing, genetically modified mice, and organoid assays. Results: We found that in the adult intestinal epithelium Id2 is predominantly expressed in enterochromaffin and peptidergic enteroendocrine cells. Consistently, the loss of Id2 leads to the reduction of Chromogranin A-positive enteroendocrine cells. In contrast, the numbers of tuft cells are increased in Id2 mutant small intestine. Moreover, ablation of Id2 elevates the numbers of Serotonin+ enterochromaffin cells and Ghrelin+ X-cells in the posterior part of the small intestine. Finally, Id2 acts downstream of BMP signalling during the differentiation of Glucagon Like Peptide-1+ L-cells and Cholecystokinin+ I-cells towards Neurotensin+PYY+ N-cells. Conclusion: Id2 plays an important role in cell fate decisions in the adult small intestine. Firstly, ID2 suppresses the differentiation of secretory intestinal epithelial progenitors towards tuft cell lineage and thus controls host immune response on commensal and parasitic microbiota. Next, ID2 is essential for establishing a differentiation gradient for enterochromaffin and X-cells along the anterior-posterior axis of the gut. Finally, ID2 is necessary for the differentiation of N-cells thus ensuring a differentiation gradient along the crypt-villi axis.

2022-06-21 | GSE178586 | GEO

In vivo CRISPR screening reveals nutrient signaling processes underpinning CD8+ T cell fate decisions [microarray_dataset1]

Project description:The role of nutrient signaling processes in the fate decision of CD8 is incompletely understood. By performing in vivo pooled CRISPR-Cas9 screening, we uncovered nutrient signaling processes underpinning the dynamics and heterogeneity of CD8 T cell fate decisions.

2021-02-25 | GSE148681 | GEO

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