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Transcriptional profile of Th17 cells: The role of glycolysis

ABSTRACT: Transcriptional profile of Th17 cells: The role of glycolysis

PROVIDER: PRJNA474607 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7262942.fastq.gz	Fastqsanger.gz
	SRR7262943.fastq.gz	Fastqsanger.gz
	SRR7262944.fastq.gz	Fastqsanger.gz
	SRR7262945.fastq.gz	Fastqsanger.gz
	SRR7262946.fastq.gz	Fastqsanger.gz

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Transcriptional profile of Th17 cells: The role of glycolysis

Project description:The aim of this study is to investigate a role of glycolysis in transcriptional programing of Th17 cells during differentiation. Naïve CD4 T cells were differentiated towards Th17 cells with or without a mild inhibition of glycolysis, and transcriptome signature was analyzed. We found about 200 transcripts were differentially regulated. Further pathway analysis suggested that glycolysis controls genes associated with IL-2/STAT5 signaling during Th17 differentiation. Inhibition of glycolysis resulted in enrichment of genes associated with translational processes and Th17 signature genes.

2020-06-01 | GSE115339 | GEO

Transcriptional regulation of Th17 differentiation by mitochondrial oxidative phosphorylation

Project description:We found that mitochondrial oxidative phosphorylation (OXPHOS) plays a critical role in Th17 lineage specification. CD4 T cells differentiated under OXPHOS inhibited conditions show altered metabolic gene profiles (mitochondrial function, glycolysis, and TCA cycle) and pathways associated with cell proliferation. Furthermore, gene set enrichment analysis (GSEA) revealed that mitochondrial respiration impacts transcriptional profiles related to Th17 pathogenic signatures and BATF-sensitive gene clusters. Our study reveals a regulatory role of mitochondrial OXPHOS in transcriptional programming of Th17 lineage commitment.

2020-01-28 | GSE115282 | GEO

Inhibition of glycolysis in pathogenic TH17 cells through targeting a miR-21-Peli1-c-Rel pathway prevents autoimmunity

Project description:It is well known that some pathogenic cells have enhanced glycolysis, the regulatory network leading to increased glycolysis are not well characterized. Here, we show that CNS-infiltrated pathogenic TH17 cells from diseased mice specifically upregulate glycolytic pathway genes compared to homeostatic intestinal TH17 cells. Bioenergetic assay and metabolomics analyses indicate that in vitro derived pathogenic TH17 cells are highly glycolytic compared to nonpathogenic TH17 cells. Chromatin landscape analyses demonstrate TH17 cells in vivo show distinct chromatin states, and pathogenic TH17 cells show enhanced chromatin accessibility at glycolytic genes with NF-kB binding sites. Mechanistic studies reveal that miR-21 targets the E3 ubiquitin ligase Peli1-c-Rel pathway to promote glucose metabolism of pathogenic TH17 cells. Therapeutic targeting c-Rel-mediated glycolysis in pathogenic TH17 cells represses autoimmune diseases. These findings extend our understanding of the regulation TH17 cell glycolysis in vivo and provide insights for future therapeutic intervention to TH17 cell mediated autoimmune diseases.

2020-04-01 | GSE127768 | GEO

Role of Ikaros in the transcriptional signature of Th17 cells

Project description:Role of Ikaros in the transcriptional signature of Th17 cells

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Role of Stat3 phosphorylation in Th17 differentiation

Project description:Determine the role of stat3 phosphorylation, particularly at S727, during the differentiation of Th17 cells.

2025-10-29 | PXD059588 | Pride

Investigating the role of STAT3 in Th17 differentiation

Project description:Our lab is working to understand the role of STAT3 and the phosphorylation at S727 in Th17 cell differentiation

2025-10-29 | PXD065517 | Pride

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

Transcriptional signature of human pro-inflammatory TH17 cells [TH17 clones]

Project description:Transcriptional signature of human pro-inflammatory TH17 cells [TH17 clones]

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CIP2A negatively regulates Th17 differentiation

Project description:Interleukin 17 (IL-17) producing T helper 17 (Th17) cells are critical drivers of pathogenesis in a variety of autoimmune and inflammatory diseases. Strategies to mitigate excessive Th17 response thus remain an attractive target for immunotherapies. Here we report that Cancerous Inhibitor of Protein Phosphatase 2A (CIP2A) regulates IL-17 production by Th17 cells in human and mouse. Using CIP2A knock-out (KO) mice and siRNA-mediated CIP2A silencing in human primary CD4+ T cells, we demonstrated that CIP2A silencing results in a significant increase in IL-17 production. Interestingly, CIP2A deficient Th17 cells were characterized by increased strength and duration of STAT3 (Y705) phosphorylation. Genome-wide gene expression profile as well as the p-STAT3 (Y705) interactome of CIP2A deficient Th17 cells identified that CIP2A regulates the strength of the interaction between Acylglycerol kinase (AGK) and STAT3, and thereby, modulates STAT3 phosphorylation as well as expression of IL-17 in Th17 cells. Our results uncover the physiological function of CIP2A in Th17 cells and provides new opportunities for therapeutic intervention in Th17 cell mediated diseases.

2020-05-26 | PXD010612 | Pride

Gene expression profile of human Th17 cells

Project description:Gene expression profile of human Th17 cells

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