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Eomes broadens the scope of CD8 T cell memory by inhibiting apoptosis in low-affinity cells

ABSTRACT: Eomes broadens the scope of CD8 T cell memory by inhibiting apoptosis in low-affinity cells

PROVIDER: PRJNA484766 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7647984.fastq.gz	Fastqsanger.gz
	SRR7647985.fastq.gz	Fastqsanger.gz
	SRR7647986.fastq.gz	Fastqsanger.gz
	SRR7647987.fastq.gz	Fastqsanger.gz
	SRR7647988.fastq.gz	Fastqsanger.gz

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Similar Datasets

Eomes broadens the scope of CD8 T cell memory by inhibiting apoptosis in low-affinity cells

Project description:The memory CD8 T cell pool must select for high-affinity clones to efficiently counter re-infection yet must retain a level of clonal diversity to allow recognition of pathogens with mutated immuno-dominant epitopes. How this is mediated is unclear, especially in the context of a selective drive for antigen-affinity. We find that low-affinity memory exclusively depends on the transcription factor Eomes in the first days after antigen encounter. Eomes is induced at low activating signal strength and directly drives transcription of the pro-survival protein Bcl-2. At higher signal intensity T-bet is induced which suppresses Bcl-2, generating a survival advantage for low-affinity cells. High-affinity cells form memory independent of Eomes and have a proliferative advantage over low-affinity cells, which compensates for their survival deficit. Thus, we demonstrate on a molecular level how sufficient diversity of the memory pool is established in an environment of affinity-based selection.

2020-08-01 | GSE118174 | GEO

Eomes broadens the scope of CD8 T-cell memory by inhibiting apoptosis in cells of low affinity.

Project description:The memory CD8 T-cell pool must select for clones that bind immunodominant epitopes with high affinity to efficiently counter reinfection. At the same time, it must retain a level of clonal diversity to allow recognition of pathogens with mutated epitopes. How the level of diversity within the memory pool is controlled is unclear, especially in the context of a selective drive for antigen affinity. We find that preservation of clones that bind the activating antigen with low affinity depends on expression of the transcription factor Eomes in the first days after antigen encounter. Eomes is induced at low activating signal strength and directly drives transcription of the prosurvival protein Bcl-2. At higher signal intensity, T-bet is induced which suppresses Bcl-2 and causes a relative survival advantage for cells of low affinity. Clones activated with high-affinity antigen form memory largely independent of Eomes and have a proliferative advantage over clones that bind the same antigen with low affinity. This causes high-affinity clones to prevail in the memory pool, despite their relative survival deficit. Genetic or therapeutic targeting of the Eomes/Bcl-2 axis reduces the clonal diversity of the memory pool, which diminishes its ability to respond to pathogens carrying mutations in immunodominant epitopes. Thus, we demonstrate on a molecular level how sufficient diversity of the memory pool is established in an environment of affinity-based selection.

| S-EPMC7077837 | biostudies-literature

NAA enhances cell yields by inhibiting apoptosis pathway

Project description:NAA enhances cell yields by inhibiting apoptosis pathway

| PRJNA1027747 | ENA

MESO-SCOPE, SCOPE cruise July 2017

Project description:MESO-SCOPE, SCOPE cruise July 2017 Raw sequence reads

| PRJNA981211 | ENA

Tbet-Eomes

Project description:Tbet-Eomes

| PRJNA706657 | ENA

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

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

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

Tbet vs Eomes [RNA-Seq]

Project description:T-bet and Eomes are related T-box transcription factors that control NK cell development. This study was designed to understand the specific roles of Eomes and T-bet in regulating gene expression. RNAseq data were generated for immature (CD11b- CD27+) and mature (CD11b+ CD27-) NK cells from T-bet KO (Tbet Ho) or control mice (Tbet WT) or from Eomes KO (Eomes Ho) or control mice (NK-Cre). Three samples were generated for each condition (Tri 1, 2, 3).

2021-05-10 | GSE168240 | GEO

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

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