Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mus musculus

ABSTRACT: Exhaustion-associated regulatory regions in CD8+ tumor-infiltrating T cells (ATAC-seq for in-vivo experiments)

PROVIDER: PRJNA359374 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR5135110_1.fastq.gz	Fastqsanger.gz
	SRR5135110_2.fastq.gz	Fastqsanger.gz
	SRR5135120_1.fastq.gz	Fastqsanger.gz
	SRR5135120_2.fastq.gz	Fastqsanger.gz
	SRR5135111_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 38

Similar Datasets

Mus musculus

Project description:Exhaustion-associated regulatory regions in CD8+ tumor-infiltrating T cells (ATAC-seq for in-vitro experiments)

| PRJNA359351 | ENA

Exhaustion-associated regulatory regions in CD8+ tumor-infiltrating T cells

Project description:Exhaustion-associated regulatory regions in CD8+ tumor-infiltrating T cells

| PRJNA359370 | ENA

Mus musculus

Project description:Exhaustion-associated regulatory regions in CD8+ tumor-infiltrating T cells (OT-I vs P14 RNA-seq)

| PRJNA359356 | ENA

Mus musculus

Project description:Exhaustion-associated regulatory regions in CD8+ tumor-infiltrating T cells (anti-PD-L1 vs Control IgG RNA-seq)

| PRJNA359369 | ENA

CD8+ T cell-derived Fgl2 regulates immunity in a cell-autonomous manner

Project description:The regulatory circuits dictating CD8+ T cell responsiveness vs. exhaustion during anti-tumor immunity are incompletely understood. Here, we report that tumor-infiltrating antigen-specific PD-1+ TCF-1- CD8+ T cells express the immunosuppressive cytokine Fgl2. Conditional deletion of Fgl2 from antigen-specific CD8+ T cells prolonged CD8+ T cell persistence, decreased phenotypic and transcriptomic signatures of T cell exhaustion, and improved tumor control. Melanoma patients who died of their disease exhibited increased expression of Fgl2 in tumor-infiltrating CD8+ T cells as compared to those who survived. PD-1+CD8+ T cell-derived Fgl2 also negatively regulated virus-specific T cell responses in a model of chronic viral infection. Mechanistically, the enhanced responsiveness of Fgl2-deficient CD8+ T cells is underpinned by the interaction of Fgl2 with CD8+ T cell-expressed FcγRIIB, ligation of which results in caspase 3/7-mediated apoptosis. These data illuminate a novel cell-autonomous regulatory axis by which PD-1+ CD8+ T cell responses are regulated in vivo.

2024-01-05 | GSE252556 | GEO

Chromatin accessibility analysis of tumor-infiltrating CD8+ T cells from tumor-bearing mice transferred Nrf2-deficient CD8+ T cells. [ATACseq]

Project description:To identify unique chromatin regions predicting the anti-tumor efficacy of Nrf2-deleted smart CD8+ T cell therapy, we performed an assay for transposase-accessible chromatin sequencing (ATAC-seq) using tumor-infiltrating CD8+ T cells from tumor-bearing mice transferred Nrf2-deficient CD8+ T cells. From the analysis of ATAC-seq data, we identified quantitatively distinct open regions of chromatin that distinguish Nrf2-deficient CD8+ T cells or WT CD8+ T cells.

2024-04-01 | GSE229990 | GEO

TET2-mutant clonal hematopoiesis prevents T-cell exhaustion and suppresses cancer metastasis [RNA-seq]

Project description:TET2-mutant clonal hematopoiesis (CH) is associated with reduced cancer metastasis in human cohorts. Using mouse models of colorectal cancer liver metastasis, we demonstrate that Tet2-deficient hematopoietic cells suppress metastatic tumor burden by preventing CD8+ T-cell exhaustion. Bulk RNA-seq of sorted CD4+ and CD8+ tumor-infiltrating lymphocytes (TILs) from Vav1CreTet2KO, Cd4CreTet2KO, and Tet2fl/fl control mice was performed to characterize transcriptional changes associated with Tet2 loss in tumor-infiltrating T cells.

2026-04-17 | GSE327454 | GEO

3D genome of CD8+ T cells reveals IRF8-mediated exhaustion in cancer

Project description:CD8+ T cell responses are essential for anti-tumor immunity, but chronic antigen exposure in cancer can lead to T cell exhaustion, marked by high PD-1 expression. Recent studies have identified progenitor-like CD8+ T cells (Tprog cells) within tumor-infiltrating lymphocytes (TILs) that sustain antitumor responses. These cells can differentiate into terminally exhausted cells (Tterm cells), losing their proliferative and effector functions. Immunotherapy aims to enhance CD8+ TILs functionality, promoting their transition from Tprog to Tterm cells. However, the mechanisms behind this exhaustion remain unclear. Single-cell RNA sequencing and ATAC-seq have revealed distinct profiles and chromatin accessibility between progenitor and terminally exhausted states. Histone modifications predict a loss of enhancer-promoter contacts during this transition. Chromatin structure plays a crucial role in T cell differentiation. We constructed a high-resolution 3D genome map of CD8+ T cell subsets and, through multi-omics integration, identified chromatin structure changes linked to T cell exhaustion, including alterations in topologically associating domains (TADs) and chromatin loops, providing new insights into the genetic basis of CD8+ T cell exhaustion in cancer.

2025-10-01 | GSE269676 | GEO

3D genome of CD8+ T cells reveals IRF8-mediated exhaustion in cancer [Hi-C]

2025-10-01 | GSE299305 | GEO

Single-cell ATAC sequencing of SIINFEKL-reactive T cells in GL261 murine brain tumors in MHC class II deficient tumor-mircoenvironments

Project description:Single cell ATAC sequencing of SIINFEKL-reactive immune cell from intracranial murine GL261-SIINFEKL tumors 20 days after inoculation. SIINFEKL-reactive T cells were sorted based on dextramer staining. We show that loss of major histocompatibility complex (MHC) class II (MHCII)-restricted antigen presentation on bbm drives dysfunctional intratumoral tumor-reactive CD8+ T cell states through increased chromatin accessibility and expression of Tox, a critical regulator of T cell exhaustion.

2023-01-11 | E-MTAB-12512 | biostudies-arrayexpress

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