Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RARa restrains CD8 T cell effector program [scRNA-seq]

ABSTRACT: ScRNA-seq for tumor-bearing RARα-KO, or RARα-TG mice bearing MC38 tumors was performed.

ORGANISM(S): Mus

PROVIDER: GSE254925 | GEO | 2025/05/14

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RARa restrains CD8 T cell effector program [bulk RNA-seq]

Project description:The roles of RARα and BATF on CD8 T cell gene expression have been determined.

2025-05-14 | GSE254923 | GEO

RARa restrains CD8 T cell effector program [CHIP-seq]

Project description:We investigated the binding of RARa and BATF to the chromatin of activated CD8 T cells. Distnctive and co-binding of the two factors in RA-depletd and replte conditions were revealed.

2025-05-14 | GSE254924 | GEO

RARa restrains CD8 T cell effector program [scRNA-seq]

Project description:RARa restrains CD8 T cell effector program [scRNA-seq]

| PRJNA1072642 | ENA

RARa restrains CD8 T cell effector program [CHIP-seq]

Project description:RARa restrains CD8 T cell effector program [CHIP-seq]

| PRJNA1072639 | ENA

RARa restrains CD8 T cell effector program [bulk RNA-seq]

Project description:RARa restrains CD8 T cell effector program [bulk RNA-seq]

| PRJNA1072640 | ENA

Krüppel-like factor 4 regulates the cytolytic effector function of exhausted CD8 T-cells [SMART-Seq]

Project description:To identify the role of KLF4 on exhausted CD8 T-cells in vivo, we adoptively transferred PmelI CD8 T-cells transduced with MigRI/Klf4 into MC38-gp100 tumor-bearing Rag2 KO mice on day7. We then isolated tumor-infiltrating PmelI CD8 T-cells on day15 and their gene expression profiles were analyzed by SMART-seq. Also, to investigate the effect of KLF4 deficiency, we isolated PD1+ CD8+ TILs from MC38 tumor-bearing control and Klf4 cKO mice on day14, and SMART-seq was performed.

2022-10-24 | GSE212803 | GEO

Impaired enolase 1 glycolytic activity restrains effector functions of tumor-infiltrating CD8+ T cells.

Project description:In the context of solid tumors, there is a positive correlation between the accumulation of cytotoxic CD8+ tumor-infiltrating lymphocytes (TILs) and favorable clinical outcomes. However, CD8+ TILs often exhibit a state of functional exhaustion, limiting their activity, and the underlying molecular basis of this dysfunction is not fully understood. Here, we show that TILs found in human and murine CD8+ melanomas are metabolically compromised with deficits in both glycolytic and oxidative metabolism. Although several studies have shown that tumors can outcompete T cells for glucose, thus limiting T cell metabolic activity, we report that a down-regulation in the activity of ENOLASE 1, a critical enzyme in the glycolytic pathway, represses glycolytic activity in CD8+ TILs. Provision of pyruvate, a downstream product of ENOLASE 1, bypasses this inactivity and promotes both glycolysis and oxidative phosphorylation, resulting in improved effector function of CD8+ TILs. We found high expression of both enolase 1 mRNA and protein in CD8+ TILs, indicating that the enzymatic activity of ENOLASE 1 is regulated posttranslationally. These studies provide a critical insight into the biochemical basis of CD8+ TIL dysfunction.

| S-EPMC6824424 | biostudies-literature

B7-H1 signaling is integrated during CD8(+) T cell priming and restrains effector differentiation.

Project description:A promising strategy in tumor immunotherapy is the use of activated dendritic cells as vehicles for tumor vaccines with the goal of activating anti-tumor T cell responses. Current formulations for dendritic cell-based immunotherapies have limited effects on patient survival, providing motivation for further investigation of ways to enhance dendritic cell priming of anti-tumor T cell responses. Using a brief in vitro priming model, we have found that B7-H1 expressed by activated dendritic cells is integrated during priming of naïve CD8(+) T cells and functions to limit the differentiation of effector T cell responses. CD8(+) T cells primed by B7-H1-deficient dendritic cells exhibit increased production of IFN-γ, enhanced target cell killing, and improved anti-tumor activity. Additionally, enhanced memory populations arise from CD8(+) T cells primed by B7-H1-deficient dendritic cells. Based on these findings, we suggest that early blockade of B7-H1 signaling should be investigated as a strategy to improve dendritic cell-based anti-tumor immunotherapy.

| S-EPMC4833388 | biostudies-literature

Tim-4+ Cavity-Resident Macrophages Impair Anti-Tumor CD8+ T cell Immunity [RNA-Seq]

Project description:Here we report RNA sequencing data from sorted Tim-4low vs Tim-4high macrophages in steady-state (no tumor) mice and also MC38-LG-tumor-bearing animals that were treated with isotype or anti-Tim-4 antibody.

2021-05-12 | GSE174151 | GEO

The effector program of human CD8 T cells supports tissue remodeling.

Project description:CD8 T lymphocytes are classically viewed as cytotoxic T cells. Whether human CD8 T cells can, in parallel, induce a tissue regeneration program is poorly understood. Here, antigen-specific assay systems revealed that human CD8 T cells not only mediated cytotoxicity but also promoted tissue remodeling. Activated CD8 T cells could produce the epidermal growth factor receptor (EGFR)-ligand amphiregulin (AREG) and sensitize epithelial cells for enhanced regeneration potential. Blocking the EGFR or the effector cytokines IFN-γ and TNF could inhibit tissue remodeling. This regenerative program enhanced tumor spheroid and stem cell-mediated organoid growth. Using single-cell gene expression analysis, we identified an AREG+, tissue-resident CD8 T cell population in skin and adipose tissue from patients undergoing abdominal wall or abdominoplasty surgery. These tissue-resident CD8 T cells showed a strong TCR clonal relation to blood PD1+TIGIT+ CD8 T cells with tissue remodeling abilities. These findings may help to understand the complex CD8 biology in tumors and could become relevant for the design of therapeutic T cell products.

| S-EPMC10791561 | biostudies-literature

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