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

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

PROVIDER: PRJNA857721 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20081507_1.fastq.gz	Fastqsanger.gz
	SRR20081507_2.fastq.gz	Fastqsanger.gz
	SRR20081508_1.fastq.gz	Fastqsanger.gz
	SRR20081508_2.fastq.gz	Fastqsanger.gz
	SRR20081509_1.fastq.gz	Fastqsanger.gz

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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

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

2023-01-18 | GSE207941 | GEO

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

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

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Regulation of Th17/Treg Balance by the Polyamine Pathway

Project description:Regulation of Th17/Treg Balance by the Polyamine Pathway

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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

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

Caffeoylquinic acids from sweetpotato (Ipomoea batatas L.) leaves ameliorates immune thrombocytopenia by regulating Th17/Treg balance

Project description:Idiopathic thrombocytopenic purpura (ITP) is an autoimmune disorder characterized by antiplatelet autoantibodies, thrombocytopenia, and bleeding, however, its treatment options are limited. In this study, a kind of active component, caffeoylquinic acid compounds from sweetpotato leaves was extracted out to explore its medicinal value and provide novel therapeutic strategies for the treatment of ITP. We isolated three compounds from the n-butanol extract of sweetpotato leaves. Caffeoylquinic acids could participate the immune balance of T-helper 17 lymphocytes (Th17) / regulatory T cells (Treg) in a murine model of ITP, which was established by injection of antiplatelet antibody. Further quantitative proteomics analysis revealed that caffeoylquinic acid could activate AMPK signaling pathway. It suggested that caffeoylquinic acid may provide a novel therapeutic strategy that relies on the AMPK pathway.

2025-01-13 | PXD059749 |

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

2011-06-07 | GSE29765 | GEO

Itaconate links inhibition of succinate dehydrogenase with macrophage metabolic remodeling and regulation of inflammation

Project description:Remodeling of the tricarboxylic acid (TCA) cycle is a metabolic adaptation mechanism accompanying inflammatory macrophage activation. During this process, endogenous metabolites can adopt regulatory roles that govern specific aspects of inflammatory response, as recently shown for succinate, which regulates the downstream pro-inflammatory IL-1Î²-HIF1a axis. Itaconate is one of the most highly induced metabolites in activated macrophages, yet its functional significance remains unknown. Here, we show that itaconate modulates macrophage metabolism and effector functions via its effect on succinate dehydrogenase, by inhibiting conversion of succinate to fumarate. Through this action, itaconate exerts anti-inflammatory effects when administered in vitro and in vivo during macrophage activation and ischemia-reperfusion injury. Using newly generated Irg1-/- mice, which lack the ability to produce itaconate, we show that endogenous itaconate regulates succinate levels and function, changes in mitochondrial respiration, and inflammatory cytokine production during macrophage activation. These studies highlight itaconate as a major physiological regulator of the global metabolic rewiring and effector functions of inflammatory macrophages. Experiment 1: mature WT BMDM were treated for 12h with 0.25 mM dimethyl itaconate (DI) or vehicle (Unst) and then stimulated with LPS (E. coli 0111:B4; 100 ng/ml, 4h) (DI+LPS; LPS); Experiment 2: mature Irg1-/- BMDM were stimulated with LPS (E. coli 0111:B4; 100 ng/ml) and murine recombinant IFNg (50 ng/ml) for 24h.

2016-07-01 | E-GEOD-82043 | biostudies-arrayexpress

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