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C-Maf-dependent Treg cell control of intestinal TH17 cells and IgA establishes host–microbiota homeostasis

ABSTRACT: c-Maf-dependent Treg cell control of intestinal TH17 cells and IgA establishes host–microbiota homeostasis

PROVIDER: PRJNA416713 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6242070_1.fastq.gz	Fastqsanger.gz
	SRR6242070_2.fastq.gz	Fastqsanger.gz
	SRR6242071_1.fastq.gz	Fastqsanger.gz
	SRR6242071_2.fastq.gz	Fastqsanger.gz
	SRR6242072_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

c-Maf-dependent Treg cell control of intestinal TH17 cells and IgA establishes host–microbiota homeostasis

Project description:Foxp3+ regulatory T (Treg) cells are essential for immunological tolerance and homeostasis. In peripheral tissues, Treg cells acquire enhanced suppressive functions and co-opt distinct transcriptional modules, allowing context and tissue-dependent immune regulation. Here we show that the transcription factor c-Maf was highly expressed by effector Treg cells and controlled their IL-10 production. In the intestine, c-Maf was required for the differentiation of RORgt+ microbiota-dependent Treg cells, and restricted their production of inflammatory cytokines. Consequently, Treg cell-specific loss of c-Maf resulted in perturbed intestinal homeostasis, microbial dysbiosis and a selective failure to control Th17 responses during homeostasis and upon chemically induced epithelial damage. Molecular profiling revealed that c-Maf regulated expression of key genes of the transcriptional signature of intestinal Treg cells, including Rorc and Il10. Thus, our study identifies a key role of c-Maf in preserving the identity and function of intestinal Treg cells, essential for the control of intestinal immune homeostasis.

2018-12-18 | GSE106396 | GEO

Human chorionic gonadotropin promotes murine Treg cells and restricts pregnancy-harmful proinflammatory Th17 responses – proteomics data

Project description:In this study, the participation of fetal factors in maintaining the immune balance during gestation was investigated by assessing the effects of human chorionic gonadotropin (hCG) on murine Treg cells and Th17 cells.

2022-10-14 | PXD035883 | Pride

Jarid2, a Polycomb member and target of miR-155, regulates the fates of Th17 and Treg cells

Project description:Genome-wide analysis of Jarid2, Suz12, and c-Maf binding and H3K27me3 profiling in miR-155 KO and WT Th17 performed by ChIP-seq. We found that Jarid2 and c-Maf is differentially expressed in absence of miR-155 and they compete for binding to the Il22 promoter. We highlight targets of Jarid2 and Suz12 in miR-155 KO Th17 cells that are epigenetically silenced by increased H3K27me3 status. Furthermore, genome-wide analysis through Suz12 ChIP-exo in WT and Jarid2fl/fl;CD4cre Th17 reveals defects in PRC2 recruitment in abscence of Jarid2 that results in derepression of genes in Th17 cells. Thus, one main function of miR-155 is to curb epigenetic silencing by targeting Jarid2. Examination of Jarid2, Suz12, c-Maf binding and H3K27me3 changes in miR-155 KO and WT Th17.

2014-06-01 | E-GEOD-47528 | biostudies-arrayexpress

The effect of dexmedetomidine on perioperative cholinergic anti-inflammatory pathway and the balance of Th17 / Treg in colorectal cancer patients

Project description:Interventions: DEX: a loading dosage of dexmedetomidine (0.5 ug/Kg) was infused introvenously 10 min before anesthesia and followed continously at0.5 ug/Kg/h for 2h;control:saline Primary outcome(s): interleukin-17, 6, 23, 10, 1ß, TNF-a, TGFß-1, HMGB1, Th17/Treg cell count Study Design: Randomized parallel controlled trial

| 2663054 | ecrin-mdr-crc

HIF1a-dependent glycolytic pathway orchestrates a metabolic checkpoint for the differentiation of TH17 and Treg cells

Project description:Upon antigen stimulation, the bioenergetic demands of T cells increase dramatically over the resting state. Although a role for the metabolic switch to glycolysis has been suggested to support increased anabolic activities and facilitate T cell growth and proliferation, whether cellular metabolism controls T cell lineage choices remains poorly understood. Here we report that the glycolytic pathway is actively regulated during the differentiation of inflammatory TH17 and Foxp3-expressing regulatory T cells (Treg), and controls cell fate determination. TH17 but not Treg-inducing conditions resulted in strong upregulation of the glycolytic activity and induction of glycolytic enzymes. Blocking glycolysis inhibited TH17 development while promoting Treg cell generation. Moreover, the transcription factor hypoxia-inducible factor 1a (HIF1a) was selectively expressed in TH17 cells and its induction required signaling through mTOR, a central regulator of cellular metabolism. HIF1a-dependent transcriptional program was important for mediating glycolytic activity, thereby contributing to the lineage choices between TH17 and Treg cells. Lack of HIF1a resulted in diminished TH17 development but enhanced Treg differentiation, and protected mice from autoimmune CNS inflammation. Our studies demonstrate that HIF1a-dependent glycolytic pathway orchestrates a metabolic checkpoint for the differentiation of TH17 and Treg cells. Naïve CD4 T cells from wild-type and HIF1a-deficient mice (in triplicates each group) were differentiated under TH17 conditions for 2.5 days, and RNA was analyzed by microarrays.

2011-06-07 | E-GEOD-29765 | biostudies-arrayexpress

Project description:c-Maf-dependent Treg cell control of intestinal TH17 cells and IgA establishes host–microbiota homeostasis

| PRJNA416946 | ENA

Itaconate regulates Th17/Treg cell balance via metabolic and epigenetic reprogramming

Project description:An imbalance of T helper (Th17) cells and regulatory T (Treg) cells contributes to the pathogenesis of autoimmune diseases. The endogenous metabolite itaconate (ITA) is a regulator of macrophages; however, its role in T cells regulation is unclear. Here, we show that ITA inhibited Th17 cell differentiation and promoted Treg cell differentiation via metabolic and epigenetic reprogramming. Mechanistically, ITA suppressed glycolysis and mitochondrial respiration in Th17 and Treg-polarizing T cells. In Th17 cells, the S-adenosyl-L-methionine/ S-adenosylhomocysteine ratio was decreased following ITA administration in vitro, subsequently altering the epigenetic status. Further, ITA inhibited RORγt binding at the Il17a promoter, resulting in reduced IL-17A expression. In Treg cells, ITA reduced 2-hydroxyglutarate levels, which suppressed Foxp3 expression. The adoptive transfer of ITA-treated Th17-polarizing T cells ameliorated experimental autoimmune encephalomyelitis. Collectively, these results indicate that ITA serves as a crucial metabolic regulator for Th17/Treg cell balance and a potential therapeutic agent against autoimmune diseases.

2023-01-18 | GSE182895 | GEO

Elucindating the role of the transcription factor IRF4 in Th17 and Treg cells

Project description:- transcription factor interferon regulatory factor 4 (IRF4) = crucial transcription factor for different immune cells, incl pro-inflammatory Th17 and anti-inflammatory Treg cells - IRF4 is essential for the cell differentiation and fate determination - however molecular mechanisms of IRF4-mediated gene expression in fully differentiated Th17/Treg cells are still not fully understood - integration of data derived from affinity-purification and full mass spectrometry-based proteome analysis with chromatin immune precipitation sequencing (ChIP-Seq) - characterization of proteins generally involved in the T cell development as well as subtype-specific differentiation and identification of novel, yet uncharted IRF4 interactors

2024-08-02 | PXD044298 | JPOST Repository

Itaconate regulates Th17/Treg cell balance via metabolic and epigenetic reprogramming [ATAC-seq]

2023-01-18 | GSE207941 | GEO

An activation-induced immunoregulatory and tissue-residency program modulated by c-MAF in human memory Th17 cells [ChIP-seq] [RNA-seq]

Project description:T cell effector function is largely mediated through the release of pro-inflammatory cytokines that need to be tightly regulated to avoid tissue damage. Here we show that the anti-inflammatory cytokine IL-10 is produced by a subset of recently-activated human Th17 cells and is controlled by the selective up-regulation of the transcription factor c-MAF. In addition, recently-activated IL-10+ Th17 cells upregulate immunoregulatory genes and genes characteristic of tissue resident T cells. In contrast, recently activated IL-10- Th17 cells maintain a pro-inflammatory gene expression profile and upregulate homing receptors to recirculate from tissues to blood. By integrating ChIP-seq and RNA-seq analyses, we demonstrate that c-MAF plays a key role in orchestrating the immune-regulatory and tissue residency program of IL-10+ Th17 cells by binding to a large number of non-promoter regions with enhancer-like features. Thus, c-MAF may represent a relevant factor discriminating between immunoregulatory and pro-inflammatory human Th17 cells.

2018-09-12 | GSE101389 | GEO

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