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Maintenance DNA methylation is essential for regulatory T cell development and stability of suppressive function [gene expression/RNA-seq]

ABSTRACT: Maintenance DNA methylation is essential for regulatory T cell development and stability of suppressive function [gene expression/RNA-seq]

PROVIDER: PRJNA602403 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10918100.fastq.gz	Fastqsanger.gz
	SRR10918101.fastq.gz	Fastqsanger.gz
	SRR10918102.fastq.gz	Fastqsanger.gz
	SRR10918103.fastq.gz	Fastqsanger.gz
	SRR10918104.fastq.gz	Fastqsanger.gz

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Maintenance DNA methylation is essential for regulatory T cell development and stability of suppressive function

Project description:Maintenance DNA methylation is essential for regulatory T cell development and stability of suppressive function

| PRJNA602400 | ENA

Maintenance DNA methylation is essential for regulatory T cell development and stability of suppressive function [DNA methylation/RRBS]

Project description:Regulatory T (Treg) cells require Foxp3 expression and induction of a specific DNA hypomethylation signature during development, after which Treg cells persist as a self-renewing population that regulates immune system activation. Whether maintenance DNA methylation is required for Treg cell lineage development and stability and how methylation patterns are maintained during lineage self-renewal remain unclear. Here, we demonstrate that the epigenetic regulator Uhrf1 is essential for maintenance of methyl-DNA marks that stabilize Treg cellular identity by repressing effector T cell transcriptional programs. Constitutive and induced deficiency of Uhrf1 within Foxp3+ cells resulted in global yet non-uniform loss of DNA methylation, derepression of inflammatory transcriptional programs, destabilization of the Treg cell lineage, and spontaneous inflammation. These findings support a paradigm in which maintenance DNA methylation is required in distinct regions of the Treg cell genome for both lineage establishment and stability of identity and suppressive function.

2020-08-27 | GSE143973 | GEO

Maintenance DNA methylation is essential for regulatory T cell development and stability of suppressive function [gene expression/RNA-seq]

2020-08-27 | GSE143972 | GEO

Maintenance DNA methylation is essential for regulatory T cell development and stability of suppressive function [DNA methylation/RRBS]

Project description:Maintenance DNA methylation is essential for regulatory T cell development and stability of suppressive function [DNA methylation/RRBS]

| PRJNA602402 | ENA

Maintenance DNA methylation is essential for regulatory T cell development and stability of suppressive function.

Project description:Tregs require Foxp3 expression and induction of a specific DNA hypomethylation signature during development, after which Tregs persist as a self-renewing population that regulates immune system activation. Whether maintenance DNA methylation is required for Treg lineage development and stability and how methylation patterns are maintained during lineage self-renewal remain unclear. Here, we demonstrate that the epigenetic regulator ubiquitin-like with plant homeodomain and RING finger domains 1 (Uhrf1) is essential for maintenance of methyl-DNA marks that stabilize Treg cellular identity by repressing effector T cell transcriptional programs. Constitutive and induced deficiency of Uhrf1 within Foxp3+ cells resulted in global yet nonuniform loss of DNA methylation, derepression of inflammatory transcriptional programs, destabilization of the Treg lineage, and spontaneous inflammation. These findings support a paradigm in which maintenance DNA methylation is required in distinct regions of the Treg genome for both lineage establishment and stability of identity and suppressive function.

| S-EPMC7710299 | biostudies-literature

Mitochondrial complex III is essential for regulatory T cell suppressive function. [DNA methylation/RRBS]

Project description:Regulatory T cells (Treg cells), a distinct subset of CD4+ T cells, are necessary for the maintenance of immune self-tolerance and homeostasis. Recent studies have demonstrated that Treg cells display a unique metabolic profile characterized by an increase in mitochondrial metabolism relative to other CD4+ effector subsets. Furthermore, the Treg cell lineage-defining transcription factor, Foxp3, has been shown to promote respiration; however, it remains unknown whether the mitochondrial respiratory chain is required for Treg cell suppressive capacity, stability, and survival. Here we report that Treg cell-specific ablation of mitochondrial respiratory chain complex III results in the development of a fatal inflammatory disease early in life, without impacting Treg cell number. Mice lacking complex III specifically in Treg cells displayed a loss of Treg cell suppressive capacity without altering Treg cell proliferation and survival. Treg cells deficient in complex III display decreased expression of genes associated with Treg function while maintaining stable FOXP3 expression. Complex III-null Treg cells displayed increased DNA methylation at the loci of differentially down-regulated genes without a global increase in DNA methylation. Loss of complex III in Treg cells resulted in buildup of the metabolites 2-hydroxyglutarate (2-HG) and succinate that can function as inhibitors of α-ketoglutarate (α−KG)-dependent dioxygenase reactions such as the ten-eleven translocation (TET) family of DNA demethylases. Thus, Treg cells require mitochondrial respiration to maintain immune regulatory gene expression and suppressive function.

2018-12-18 | GSE120451 | GEO

Mitochondrial complex III is essential for regulatory T cell suppressive function

Project description:Mitochondrial complex III is essential for regulatory T cell suppressive function

| PRJNA493083 | ENA

Mitochondrial complex III is essential for regulatory T cell suppressive function. [gene expression/RNA-seq]

2018-12-18 | GSE120449 | GEO

Maintenance DNA methylation is essential for regulatory T cell development and stability of suppressive function

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

2020-08-27 | GSE143974 | GEO

Foxp1 is critical for the maintenance of regulatory T-cell homeostasis and suppressive function

Project description:Foxp1 is critical for the maintenance of regulatory T-cell homeostasis and suppressive function

| PRJNA496482 | ENA