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Deletion of a state-specific PD-1 enhancer modulates exhausted T cell fate and function [ATAC-seq]

ABSTRACT: Deletion of a state-specific PD-1 enhancer modulates exhausted T cell fate and function [ATAC-seq]

PROVIDER: PRJNA875661 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21387164_1.fastq.gz	Fastqsanger.gz
	SRR21387164_2.fastq.gz	Fastqsanger.gz
	SRR21387165_1.fastq.gz	Fastqsanger.gz
	SRR21387165_2.fastq.gz	Fastqsanger.gz
	SRR21387166_1.fastq.gz	Fastqsanger.gz

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Deletion of a state-specific PD-1 enhancer modulates exhausted T cell fate and function

Project description:Deletion of a state-specific PD-1 enhancer modulates exhausted T cell fate and function

| PRJNA875652 | ENA

Deletion of a state-specific PD-1 enhancer modulates exhausted T cell fate and function [ATAC-seq]

Project description:T cell exhaustion is a state of CD8+ T cell dysfunction elicited by chronic exposure to antigen and inflammation, arises in both cancer and chronic viral infection. The co-inhibitory receptor PD-1 plays a key role in mediating exhaustion, but complete ablation of PD-1 by gene knock-out leads to deeper functional deficits and poor T cell survival. We hypothesized that an intermediate level of PD-1 expression may confer an improved balance of exhausted CD8+ T cell functionality, so we deleted an exhaustion-associated enhancer of PD-1 which indeed resulted in a reduced expression level. We compared EnhDel, WT and PD-1 KO T cells using single-cell RNA-Seq and found that PD-1 KO but not EnhDel cells are strongly biased towards the terminally exhausted subset. EnhDel cells also uniquely enrich for effector-associated genes and gene signatures. However, all three genotypes (EnhDel, WT and PD-1 KO) exhibit a similar chromatin accessibility landscape by ATAC-Seq, controlling for exhausted subset. These data suggest that tuning of PD-1 expression may uniquely permit the maintenance of an “effector” transcriptional profile in exhausted CD8+ T cells.

2024-07-29 | GSE212506 | GEO

Deletion of a state-specific PD-1 enhancer modulates exhausted T cell fate and function [scRNA-seq]

2024-07-29 | GSE212379 | GEO

Deletion of a state-specific PD-1 enhancer modulates exhausted T cell fate and function [RNA-Seq]

2024-07-29 | GSE269580 | GEO

Deletion of a state-specific PD-1 enhancer modulates exhausted T cell fate and function [RNA-Seq]

Project description:Deletion of a state-specific PD-1 enhancer modulates exhausted T cell fate and function [RNA-Seq]

| PRJNA1122563 | ENA

Deletion of a state-specific PD-1 enhancer modulates exhausted T cell fate and function [scRNA-seq]

Project description:Deletion of a state-specific PD-1 enhancer modulates exhausted T cell fate and function [scRNA-seq]

| PRJNA875151 | ENA

Deletion of a state-specific PD-1 enhancer modulates exhausted T cell fate and function

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

2024-07-28 | GSE212507 | GEO

Tox4 Modulates Cell Fate Reprogramming

Project description:Tox4 Modulates Cell Fate Reprogramming

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Tox4 Modulates Cell Fate Reprogramming

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Comparison of gene expression profiles of Jurkat cells with or without PD-1 ligation

Project description:CD8+ T cells in chronic viral infections like HIV develop functional defects such as loss of IL-2 secretion and decreased proliferative potential that are collectively termed exhaustion1. Exhausted T cells express increased levels of multiple inhibitory receptors, such as Programmed Death 1 (PD-1). PD-1 inhibition contributes to impaired virus-specific T cell function in chronic infection because antibody-mediated blockade of its ligand, Programmed Death Ligand 1 (PD-L1) is sufficient to improve T cell function and reduce viral replication in animal models. Reversing PD-1 inhibition is therefore an attractive therapeutic target, but the cellular mechanisms by which PD-1 ligation results in T cell inhibition are not fully understood. PD-1 is thought to limit T cell activation by attenuating T cell receptor (TCR) signaling. It is not known whether PD-1 ligation also acts by upregulating genes in exhausted T cells that impair their function. Here, we analyzed gene-expression profiles from HIV-specific CD8+ T cells in patients with HIV and show that PD-1 coordinately upregulates a program of genes in exhausted CD8+ T cells from humans and mice. This program includes upregulation of basic leucine transcription factor, ATF-like (BATF), a transcription factor in the AP-1 family. Enforced expression of BATF was sufficient to impair T cell proliferation and cytokine secretion, while BATF knockdown reduced PD-1 inhibition. Silencing BATF in CD4+ and CD8+ T cells from chronic viremic patients rescued HIV-specific T cell function. Thus inhibitory receptors can cause T cell exhaustion by upregulating genes â such as BATF â that inhibit T cell function. PD-1 expressing Jurkat cells were cultured for 18 hours with beads coated with antibodies to CD3 and CD28, with our without an antibody to PD-1.

2010-10-03 | E-GEOD-24026 | biostudies-arrayexpress

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