Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

High levels of Eomes promote exhaustion of anti-tumor CD8+ T cells

ABSTRACT: High levels of Eomes promote exhaustion of anti-tumor CD8+ T cells

PROVIDER: PRJNA506835 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR8240830.fastq.gz	Fastqsanger.gz
	SRR8240831.fastq.gz	Fastqsanger.gz
	SRR8240834.fastq.gz	Fastqsanger.gz
	SRR8240835.fastq.gz	Fastqsanger.gz
	SRR8240836.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

High Levels of Eomes Promote Exhaustion of Anti-tumor CD8+ T Cells.

Project description:Eomes, a T-box transcription factor, is known important for both function and homeostasis of effector and memory T cells, but was recently also implicated in CD8+ T cell exhaustion. However, whether and how Eomes might regulate effector functions or exhaustion of CD8+ T cells, especially in the tumor setting, is unknown. Here we first show, as tumor progressed, Eomes expression was elevated in tumor-infiltrating CD8+ T cells, especially in PD-1+Tim-3+ exhausted CD8+ T cells. Complete loss of Eomes in T cells resulted in impaired development of anti-tumor CTLs, whereas deletion of one allele of Eomes in T cells decreased development of exhausted CD8+ T cells, which offered better tumor control. Integrative analysis of RNAseq and ChIPseq of Eomes-overexpressing T cells revealed that high levels of Eomes expression directly controlled expression of T cell exhaustion genes, such as Havcr2. In addition, Eomes might compete with T-bet binding to regulatory genomic loci to antagonize T-bet functions. Collectively, Eomes exerts bimodal functions in CD8+ T cells in tumor.

| S-EPMC6305494 | biostudies-literature

anti-Eomes ChIPseq of control OT-I cells and Eomes-overexpressing OT-I cells

Project description:High amount of Eomes might drive T cell exhaustion. In order to understand how Eomes contributes to exhaustion of CD8+ T cell in the TME as a transcription factor, we conducted anti-Eomes ChIPseq analysis of control OT-I cells and Eomes-overexpressing OT-I cells.

2018-11-26 | GSE122888 | GEO

High levels of Eomes promote exhaustion of anti-tumor CD8+ T cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-11-26 | GSE122895 | GEO

RNAseq of control OT-I cells and Eomes-overexpressing OT-I cells

Project description:High amount of Eomes might drive T cell exhaustion. In order to understand how Eomes contributes to exhaustion of CD8+ T cell in the TME, we conducted transcriptional analysis of control OT-I cells and Eomes-overexpressing OT-I cells

2018-11-26 | GSE122889 | GEO

EOMES interacts with RUNX3 and BRG1 to promote innate memory cell formation through epigenetic reprogramming

Project description:Memory CD8+ T cells have the ability to provide lifelong immunity against pathogens. Although memory features generally arise after challenge with a foreign antigen, naïve CD8 single positive (SP) thymocytes may acquire phenotypic and functional characteristics of memory cells in response to cytokines such as interleukin-4. This process is associated with the induction of the T-box transcription factor Eomesodermin (EOMES). However, the underlying molecular mechanisms remain ill-defined. Using epigenomic profiling, we show that these innate memory CD8SP cells acquire only a portion of the active enhancer repertoire of conventional memory cells. This reprograming is secondary to EOMES recruitment, mostly to RUNX3-bound enhancers. Furthermore, EOMES is found within chromatin-associated complexes containing BRG1 and promotes the recruitment of this chromatin remodelling factor. Also, the in vivo acquisition of EOMES-dependent program is BRG1-dependent. In conclusion, our results support a strong epigenetic basis for the EOMES-driven establishment of CD8+ T cell innate memory program.

2019-06-06 | PXD014142 | Pride

Homeostatic PD-1 signalling restrains Eomes-dependent oligoclonal expansion of liver- resident CD8 T cells [scRNA-seq]

Project description:The coinhibitory PD-1 signalling pathway plays a major role in the context of tumor-specific T cell responses. Conversely, it also contributes to the maintenance of peripheral tolerance as patients receiving anti-PD-1 treatment are prone to developing immune-related adverse events. Yet, the physiological role of the PD-1/PDL-1 axis in T cell homeostasis is still poorly understood. Herein, we show that under steady-state conditions, the absence of PD-1 signaling led to a preferential expansion of CD8+ T cells in the liver. These cells exhibited an oligoclonal TCR repertoire and a terminally differentiated exhaustion profile with high levels of the transcription factors TOX and EOMES. Using loss- or gain-of-function strategies, we could demonstrate that EOMES was required for the clonal expansion and acquisition of this differentiation program. Furthermore, single cell transcriptomics coupled to TCR repertoire analysis strongly supported the notion that these cells arise locally from liver-resident memory CD8 T cells. With these results, we uncovered an unexpected role for PD-1 signaling in liver memory T cell homeostasis.

2023-01-15 | GSE217985 | GEO

Homeostatic PD-1 signalling restrains Eomes-dependent oligoclonal expansion of liver- resident CD8 T cells [ATAC-seq]

2023-01-15 | GSE217984 | GEO

Expression data from Eomes+ and Eomes- CD8 T cells following aOX40/aCTLA-4 treatment

Project description:Development, maturation, and function of CD8 T cells is regulated by transcription factor expression. Expression of the transcription factor Eomesodermin was found to be significantly increased in CD8 T cells following aOX40/aCTLA-4 immunotherapy in mice. We used microarray analysis to detail gene expression in Eomes+ and Eomes- CD8 T cells following aOX40/aCTLA-4 treatment to determin functional differences between these two populations.

2021-02-11 | GSE166532 | GEO

Tbet-Eomes

Project description:Tbet-Eomes

| PRJNA706657 | ENA

Methylmalonic acid induces metabolic abnormalities and exhaustion in CD8+ T cells to suppress anti-tumor immunity

Project description:Systemic levels of methylmalonic acid (MMA), a byproduct of propionate metabolism, increase with age and MMA promotes tumor progression via its direct effects in tumor cells. However, the role of MMA in modulating the tumor ecosystem remains to be investigated. The proliferation and function of CD8+ T cells, key anti-tumor immune cells, declines with age and in conditions of vitamin B12 deficiency, which are the two most well-established conditions that lead to increased systemic levels of MMA. Thus, we hypothesized that increased circulatory levels of MMA would lead to a suppression of CD8+ T cell immunity. Treatment of primary CD8+ T cells with MMA induced a dysfunctional phenotype characterized by robust immunosuppressive transcriptional reprogramming and marked increases in the expression of the exhaustion regulator, TOX. Accordingly, MMA treatment upregulated exhaustion markers in CD8+ T cells and decreased their effector functions, which drove the suppression of anti-tumor immunity in vitro and in vivo. Mechanistically, MMA-induced CD8+ T cell exhaustion was associated with a suppression of NADH-regenerating reactions in the TCA cycle and concomitant defects in mitochondrial function. Thus, MMA has immunomodulatory roles, thereby highlighting MMA as an important link between aging, immune dysfunction, and cancer.

2024-10-17 | GSE256487 | 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