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PRMT5 deficiency enforces the transcriptional and epigenetic programs of Klrg1+CD8+ terminal effector T cells [scRNA-seq]

ABSTRACT: PRMT5 deficiency enforces the transcriptional and epigenetic programs of Klrg1+CD8+ terminal effector T cells [scRNA-seq]

PROVIDER: PRJNA775082 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16597300_1.fastq.gz	Fastqsanger.gz
	SRR16597300_2.fastq.gz	Fastqsanger.gz
	SRR16597301_1.fastq.gz	Fastqsanger.gz
	SRR16597301_2.fastq.gz	Fastqsanger.gz
	SRR16597302_1.fastq.gz	Fastqsanger.gz

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PRMT5 deficiency enforces the transcriptional and epigenetic programs of Klrg1+CD8+ terminal effector T cells [CHIP-seq]

Project description:Protein arginine methyltransferase 5 (PRMT5) participates in symmetric dimethylation of arginine residues of proteins and contributes to a wide range of biological processes. But how PRMT5 affects the transcriptional and epigenetic programs involved in the establishment and maintenance of T cell subsets differentiation and roles in antitumor immunity are still incompletely understood. Here, using the single cell RNA sequencing, CHIP-sequencing and bulk RNA sequencing, we found that mice T cell-specific deletion of PRMT5 had greater effects on CD8+ than CD4+ T cells development, enforcing CD8+ T cells differentiation into Klrg1+ terminal effector cells. Mechanically, T cells deficiency of PRMT5 activated Prdm1 by decreasing H4R3me2s and H3R8me2s deposition on its loci, which promote differentiation of Klrg1+CD8+ T cells. Furthermore, effector CD8+ T cells that transited into memory precursor cells were decreased in PRMT5 deficiency T cells thus caused dramatic CD8+ T cells death.

2021-11-02 | GSE186850 | GEO

PRMT5 deficiency enforces the transcriptional and epigenetic programs of Klrg1+CD8+ terminal effector T cells [scRNA-seq]

2021-11-02 | GSE186699 | GEO

PRMT5 deficiency enforces the transcriptional and epigenetic programs of Klrg1+CD8+ terminal effector T cells [RNA-seq]

2021-11-02 | GSE186851 | GEO

PRMT5 deficiency enforces the transcriptional and epigenetic programs of Klrg1+CD8+ terminal effector T cells

Project description:PRMT5 deficiency enforces the transcriptional and epigenetic programs of Klrg1+CD8+ terminal effector T cells

| PRJNA776519 | ENA

PRMT5 deficiency enforces the transcriptional and epigenetic programs of Klrg1+CD8+ terminal effector T cells [RNA-seq]

Project description:PRMT5 deficiency enforces the transcriptional and epigenetic programs of Klrg1+CD8+ terminal effector T cells [RNA-seq]

| PRJNA776290 | ENA

PRMT5 deficiency enforces the transcriptional and epigenetic programs of Klrg1+CD8+ terminal effector T cells [CHIP-seq]

Project description:PRMT5 deficiency enforces the transcriptional and epigenetic programs of Klrg1+CD8+ terminal effector T cells [CHIP-seq]

| PRJNA776287 | ENA

PRMT5 deficiency enforces the transcriptional and epigenetic programs of Klrg1+CD8+ terminal effector T cells

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

2021-11-01 | GSE186863 | GEO

RNA-sequencing of three murine memory CD8 T cell subsets: IL-7Rα+KLRG1- , IL-7Rα+KLRG1+, and IL-7Rα-KLRG1+

Project description:The goal of this study is to characterize the transcriptional profile of three memory CD8 T cell subsets: IL-7Rα+KLRG1- (memory precursors, MP), IL-7Rα+KLRG1+ (KLRG1+ MP) and IL-7Rα-KLRG1+ (terminal effectors, TE).

2022-12-12 | GSE218777 | GEO

Circulating KLRG1+ memory T cells retain the flexibility to become tissue-resident

Project description:KLRG1+ CD8 T cells persist for months after clearance of acute infections and maintain high levels of effector molecules, contributing protective immunity against systemic pathogens. Upon secondary infection, these long-lived effector cells (LLECs) are incapable of forming other circulating KLRG1− memory subsets such as central and effector memory T cells. Thus, KLRG1+ memory T cells are frequently referred to as a terminally differentiated population that is relatively short lived. Here, we show that following viral infection of mice, effector cells derived from LLEC rapidly enter nonlymphoid tissues and reduce pathogen burden, but are largely dependent on receiving antigen cues from vascular endothelial cells. Single-cell RNA sequencing revealed that secondary memory cells in nonlymphoid tissues arising from either KLRG1+ or KLRG1− memory precursors developed a similar transcriptional signature. Thus, although LLEC cannot differentiate into other circulating memory populations, they still retain the flexibility to enter tissues and establish residency.

2025-03-05 | GSE261279 | GEO

KLRG1+ Memory CD8 T cells Combine Properties of Short-lived Effectors and Long-lived Memory

Project description:CD8 effector T cells with a CD127hi KLRG1- phenotype are considered precursors to the long-lived memory pool, while KLRG1+ CD127low cells are viewed as short-lived effectors. Nevertheless, we and others have shown that a KLRG1+ CD127low population persists into the memory phase and that these T cells (termed long-lived effector cells or LLEC) display robust protective function during acute re-challenge with bacteria or viruses. Whether these T cells represent a true memory population or are instead a remnant effector cell population that failed to undergo initial contraction has remained unclear. Here, we show that LLEC from mice express a distinct phenotypic and transcriptional signature that shares characteristics of both early effectors and long-lived memory cells. Furthermore, we find that LLEC are exclusively derived from day 12 KLRG1+ effector cells. Our work challenges the concept that the KLRG1+ CD127low population is dominated by short-lived cells and shows that KLRG1 downregulation is not a prerequisite to become a long-lived protective memory T cell.

2020-08-26 | GSE152841 | GEO

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