Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Eomes regulates mitochondrial function and promotes survival of pathogenic CD4+ T cells during chronic inflammation [CUT&RUN]

ABSTRACT: Eomes regulates mitochondrial function and promotes survival of pathogenic CD4+ T cells during chronic inflammation [CUT&RUN]

PROVIDER: PRJNA1040833 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR26841594_1.fastq.gz	Fastqsanger.gz
	SRR26841594_2.fastq.gz	Fastqsanger.gz
	SRR26841595_1.fastq.gz	Fastqsanger.gz
	SRR26841595_2.fastq.gz	Fastqsanger.gz
	SRR26841596_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Eomes regulates mitochondrial function and promotes survival of pathogenic CD4+ T cells during chronic inflammation [CUT&RUN]

Project description:The tissue accumulation of T cells expressing the transcription factor Eomesodermin (Eomes) has been reported in several chronic inflammatory diseases, including multiple sclerosis. However, the mechanisms whereby Eomes controls this accumulation and strengthens inflammation remains ill-defined. Here, we show that Eomes deletion in antigen-specific CD4+ T cells is sufficient to protect against central nervous system (CNS) inflammation. We demonstrate that Eomes is dispensable for the initial priming of CD4+ T cells but is required for long-term maintenance of CNS-infiltrating CD4+ T cells. Our transcriptomic studies reveal that the impact Eomes on effector CD4+ T cell longevity is associated with sustained expression of multiple genes involved in mitochondrial organization and function. Accordingly, epigenetic studies demonstrate that Eomes supports mitochondrial function by direct binding to either metabolism-associated genes or mitochondrial transcriptional modulators. Besides, the significance of these findings was confirmed in both healthy donors and multiple sclerosis patients. CD4+ T cells expressing Eomes exhibit enhanced mitochondrial functions, which resulted in their increased capacity to survive upon prolonged in vitro stimulation. Together, our data reveal a new mechanism by which Eomes promotes severity and chronicity of inflammation via the enhancement of CD4+ T cell mitochondrial functions and resistance to stress-induced cell death.

2023-12-23 | GSE247861 | GEO

Eomes regulates mitochondrial function and promotes survival of pathogenic CD4+ T cells during chronic inflammation

Project description:Eomes regulates mitochondrial function and promotes survival of pathogenic CD4+ T cells during chronic inflammation

| PRJNA1040826 | ENA

Eomes regulates mitochondrial function and promotes survival of pathogenic CD4+ T cells during chronic inflammation [ATAC-seq]

2023-12-23 | GSE247860 | GEO

Eomes regulates mitochondrial function and promotes survival of pathogenic CD4+ T cells during chronic inflammation [RNA-seq]

2023-12-23 | GSE247862 | GEO

Eomes regulates mitochondrial function and promotes survival of pathogenic CD4+ T cells during chronic inflammation [RNA-seq]

Project description:Eomes regulates mitochondrial function and promotes survival of pathogenic CD4+ T cells during chronic inflammation [RNA-seq]

| PRJNA1040834 | ENA

Eomes regulates mitochondrial function and promotes survival of pathogenic CD4+ T cells during chronic inflammation [ATAC-seq]

Project description:Eomes regulates mitochondrial function and promotes survival of pathogenic CD4+ T cells during chronic inflammation [ATAC-seq]

| PRJNA1040832 | ENA

Eomes-dependent mitochondrial regulation promotes survival of pathogenic CD4+ T cells during inflammation.

Project description:The mechanisms whereby Eomes controls tissue accumulation of T cells and strengthens inflammation remain ill-defined. Here, we show that Eomes deletion in antigen-specific CD4+ T cells is sufficient to protect against central nervous system (CNS) inflammation. While Eomes is dispensable for the initial priming of CD4+ T cells, it is required for long-term maintenance of CNS-infiltrating CD4+ T cells. We reveal that the impact of Eomes on effector CD4+ T cell longevity is associated with sustained expression of multiple genes involved in mitochondrial organization and functions. Accordingly, epigenetic studies demonstrate that Eomes supports mitochondrial function by direct binding to either metabolism-associated genes or mitochondrial transcriptional modulators. Besides, the significance of these findings was confirmed in CD4+ T cells from healthy donors and multiple sclerosis patients. Together, our data reveal a new mechanism by which Eomes promotes severity and chronicity of inflammation via the enhancement of CD4+ T cell mitochondrial functions and resistance to stress-induced cell death.

| S-EPMC10772920 | biostudies-literature

Gene expression of sorted Eomes+ and Eomes‒ γδ T cells from spleen of Eomes-IRES-GFP mice.

Project description:Eomesodermin (Eomes) is a transcription factor with a crucial role regulating cytotoxic function, development and survival of immune cells. Although it is known that γδ T cells can express Eomes, its function on those cells is still largely unknown. Using Eomes-IRES-GFP mice we were able to sort for Eomes+ and Eomes‒ γδ T cells populations and get their gene expression profiles, bringing light to the role of Eomes on γδ T cells.

2017-04-10 | GSE85585 | GEO

EOMES safeguards TSC chromatin accessibility by directing BRG1 to TSC-associated loci [CUT&RUN]

Project description:EOMES safeguards TSC chromatin accessibility by directing BRG1 to TSC-associated loci [CUT&RUN]

| PRJNA1154558 | ENA

Targets of EOMES in mouse CD4+ T cells

Project description:To gain mechanistic insights into how EOMES regulates CD4+ T-cell differentiation and function, we performed an RNA-seq analysis using Eomes-GFP reporter mice (Eomes+/GFP) to isolate GFP+ (EOMES+) and GFP- (EOMES-) CD4+ T-cells by FACS sorting. We also sequenced RNA from Eomes-deficient GFP+ and GFP- CD4+ T-cells isolated from EomesΔT/GFP knock-out mice, in which one Eomes allele is disrupted by GFP insertion and the DNA-binding domain of the other allele is deleted in T cells by Lck-driven Cre recombinase. Hence, we had two populations of GFP+ cells where the EOMES locus was transcribed, one with a transcriptionally active EOMES protein (Eomes+/GFP) and another one with no transcriptionally active EOMES (EomesΔT/GFP), plus the respective GFP-negative controls isolated from the same mice. A homogeneous population of EOMES-expressing CD4+ T cells were obtained by transferring naïve sorted CD25- CD45RBhigh CD4+ T-cells isolated from Eomes+/GFP reporter or EomesΔT/GFP knock-out donor animals into Rag2-/- mice. After three weeks of adoptive transfer GFP+ and GFP- CD4+ T-cell populations from these mice were FACS-sorted for transcriptome analysis by RNA sequencing.

2020-10-01 | GSE145145 | 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