Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mapping self-associating chromatin hubs identifies Id proteins as key determinants of exhausted T cell fate

ABSTRACT: The goal of this study is to determine how transcription cofactors, Id2 and Id3, mediate differential regulation of exhausted CD8 T cell fate decision and differentiation at the early stage of responses to chronic viral infection.

ORGANISM(S): Mus musculus

PROVIDER: GSE310256 | GEO | 2026/04/15

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Mapping self-associating chromatin hubs identifies Id proteins as key determinants of exhausted T cell fate

Project description:This study aims to define how Id2 and Id3 regulate exhausted CD8+ T cell fate. We found that Id2 deletion reduced the Tex-eff population, whereas Id3 ablation in CD4-Cre mice diminished Tpex cells, indicating subset-specific roles for Id2 and Id3. Mechanistically, E2A is a major target of Id2/3, and Runx3 interacts with E2A. Pulldown of Id2/3 recovered both E2A and Runx3, supporting an Id2/3?E2A?Runx3 regulatory complex. To map the genomic occupancy of Id2 and Id3, we expressed 3×T7-tagged Id2 or Id3 in in vitro-primed CD45.2+ P14 cells, adoptively transferred these cells into CD45.1 recipient mice, and infected the recipients with LCMV Clone 13. On day 6 post-infection, Tex-eff and Tpex cells were isolated for T7 CUT&RUN to define Id2 binding in Tex-eff cells and Id3 binding in Tpex cells, with the empty T7 vector backbone used as a negative control.

2026-04-20 | GSE310322 | GEO

Mapping self-associating chromatin hubs identifies Id proteins as key determinants of exhausted T cell fate

Project description:Mapping self-associating chromatin hubs identifies Id proteins as key determinants of exhausted T cell fate

| PRJNA1365524 | ENA

Mapping self-associating chromatin hubs identifies Id proteins as key determinants of exhausted T cell fate

Project description:Mapping self-associating chromatin hubs identifies Id proteins as key determinants of exhausted T cell fate

| PRJNA1365760 | ENA

A genetic circuitry linking Id-proteins (Id2 and Id3) and the AKT-FOXO-mTORC1 axis to suppress innate-variant TFH cell development, maintain T cell quiescence and prevent lymphomagenesis.

Project description:It is now well established that the E- and Id-protein axis regulates multiple steps in lymphocyte development. However, it remains unknown as to how E- and Id-proteins mechanistically enforce and maintain the naïve T cell fate. Here we show that Id2 and Id3 suppressed the development and expansion of innate-variant TFH cells. Innate-variant TFH cells required MHC Class I-like signalling and were associated with germinal center B cell development. We found that Id2 and Id3 induced Foxo1 and Foxp1 expression to antagonize the activation of TFH transcription signature. We show that Id2 and Id3 acted upstream of the Hif1a/Foxo/AKT/mTORC1 pathway as well as the c-myc/p19Arf module to control cellular expansion and activation. We found that mice depleted for Id2 and Id3 expression developed colitis and αβ T cell lymphomas. Lymphomas depleted for Id2 and Id3 expression displayed elevated levels of c-myc whereas p19Arf abundance declined. Transcription signatures of Id2- and Id3-depleted lymphomas revealed similarities with genetic deficiencies associated with Burkitt lymphoma. We propose that in response to antigen receptor and/or cytokine signaling the E-Id protein axis modulates the activities of the PI3K-AKT-mTORC1-Hifa and c-myc/p19Arf pathways to control cellular expansion and homeostatic proliferation. RNA-seq data of 5 of wild type CD4SP cells, 3 of wild type Tfh cells, 3 of Id3-/- CD4SP cells, 3 of Id2-/-Id3-/-(dKO) CD4SP cells, and 6 of Id2-/-Id3-/- lymphoma cells.

2015-03-04 | E-GEOD-64779 | biostudies-arrayexpress

The Id-RAP1 axis is essential for glioma maintenance and residency of glioma cells in the perivascular niche

Project description:The experiment was designed to achieve Cre recombinase mediated deletion of Id1, Id2 and Id3 in a temporally controlled fashion in tumor cells of Id1, Id2, Id3 floxed mice with the aim of comparing the gene expression profiles of Id expressing versus Id deleted tumors.

2013-04-30 | E-MTAB-1303 | biostudies-arrayexpress

A genetic circuitry linking Id-proteins (Id2 and Id3) and the AKT-FOXO-mTORC1 axis to suppress innate-variant TFH cell development, maintain T cell quiescence and prevent lymphomagenesis.

2015-03-04 | GSE64779 | GEO

Single-cell RNA-seq of human breast tumor samples with exhausted and non-exhausted immune environments

Project description:Fresh human breast tumor tissue was dissociated into single cells and viably frozen. Patient samples were annotated as having an ""exhausted"" or ""non-exhausted"" immune environment based on CyTOF characterization of T cell phenotypes (Wagner et al, Cell 2019). 14 samples (7 exhausted, 7 non-exhausted) were selected for scRNA-seq (without prior cell type enrichment) with the goal to compare the two immune environment types and to comprehensively characterize exhaustion-associated features of the tumor microenvironment.

2023-08-25 | E-MTAB-10607 | biostudies-arrayexpress

Id proteins suppress E2A-driven iNKT cell development prior to TCR selection [RNA-seq_new]

Project description:Id proteins have been shown to promote the differentiation of conventional αβ and γδT cells, and to suppress the expansion of invariant Natural Killer T (iNKT) cells and innate-like γδNKT within their respective cell lineages. However, it remains to be determined whether Id proteins regulate lineage specification in developing T cells that give rise to these distinct cell fates. Here we report that in the absence of Id2 and Id3 proteins, E2A prematurely activates genes critical for the iNKT cell lineage prior to TCR expression. Lack of Id proteins also promotes a biased TCR rearrangement in favor of iNKT cell fate prior to selection at the CD4+CD8+ double positive (DP) stage. Enhanced iNKT development in Id3-deficient mice lacking γδNKT cells suggests that Id3 regulates the lineage competition between these populations. RNA-Seq analysis establishes E2A as the transcriptional regulator of both iNKT and γδNKT development. In the absence of pre-TCR signaling, Id2/Id3 deletion gives rise to a large population of iNKT cells and a unique innate-like DP population, despite the block in conventional αβ T cell development. The transcriptional profile of these unique DP cells reflects enrichment of innate-like signature genes, including PLZF (Zbtb16) and Granzyme A (Gzma). Results from these genetic models and genome-wide analyses suggest that Id proteins suppress E2A-driven innate-like T cell programs prior to TCR selection to enforce predominance of conventional T cells.

2018-01-23 | GSE100601 | GEO

Id proteins suppress E2A-driven iNKT cell development prior to TCR selection [RNA-seq]

2018-01-23 | GSE89848 | GEO

Id proteins suppress E2A-driven iNKT cell development prior to TCR selection [ChIP-seq]

2018-01-23 | GSE89847 | GEO