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Candida albicans-specific Th17 cell-mediated response contributes to alcohol-associated liver disease [scRNA & scTCR-seq]

ABSTRACT: Candida albicans-specific Th17 cell-mediated response contributes to alcohol-associated liver disease [scRNA & scTCR-seq]

PROVIDER: PRJNA891302 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21933433_1.fastq.gz	Fastqsanger.gz
	SRR21933433_2.fastq.gz	Fastqsanger.gz
	SRR21933434_1.fastq.gz	Fastqsanger.gz
	SRR21933434_2.fastq.gz	Fastqsanger.gz
	SRR21933435_1.fastq.gz	Fastqsanger.gz

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Candida albicans-specific Th17 cell-mediated response contributes to alcohol-associated liver disease [scRNA & scTCR-seq]

Project description:Alcohol-associated liver disease is accompanied by changes in the intestinal mycobiome. How fungal dysbiosis contributes to liver disease is not clear. T-helper (Th17) cells mediate immune responses against fungi, but the interleukin 17 (IL17) pathway has been associated with pathogenesis of alcohol-associated liver disease. Here, we demonstrate that Candida albicans (C. albicans)-specific Th17 cells are increased in the circulation and present in the liver of patients with alcohol-associated liver disease. Chronic ethanol administration to mice results in migration of C. albicans-reactive Th17 cells from the intestine to the liver. The antifungal agent nystatin reduced intestinal fungal overgrowth, decreased C. albicans-specific Th17 cells in the liver, and reduced features of ethanol-induced liver disease in mice. Transgenic mice that express a T-cell receptor (TCR) reactive to Candida antigens develop more severe ethanol-induced liver disease than transgene-negative littermates; disease severity was reduced by administration of an antibody against IL17 to the TCR transgenic mice. Adoptive transfer of C. albicans-reactive Th17 cells exacerbated ethanol-induced liver disease in wild-type mice. IL17 receptor A (IL17ra) signaling in Kupffer cells was required for the effects of C. albicans-reactive Th17 cells. Our findings indicate that ethanol increases C. albicans-reactive Th17 cells, which contribute to alcohol-associated liver disease.

2023-02-16 | GSE215930 | GEO

Candida albicans-specific Th17 cell-mediated response contributes to alcohol-associated liver disease [bulk TCR-seq]

2023-02-16 | GSE215929 | GEO

Candida albicans-specific Th17 cell-mediated response contributes to alcohol-associated liver disease

Project description:Candida albicans-specific Th17 cell-mediated response contributes to alcohol-associated liver disease

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Candida albicans-specific Th17 cell-mediated response contributes to alcohol-associated liver disease [bulk TCR-seq]

Project description:Candida albicans-specific Th17 cell-mediated response contributes to alcohol-associated liver disease [bulk TCR-seq]

| PRJNA891303 | ENA

BCL6 corepressor contributes to Th17 cell formation by inhibiting Th17 fate suppressors

Project description:BCL6 corepressor contributes to Th17 cell formation by inhibiting Th17 fate suppressors

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Candida albicans-specific Th17 cell-mediated response contributes to alcohol-associated liver disease.

Project description:Alcohol-associated liver disease is accompanied by intestinal mycobiome dysbiosis, yet the impacts on liver disease are unclear. We demonstrate that Candida albicans-specific T helper 17 (Th17) cells are increased in circulation and present in the liver of patients with alcohol-associated liver disease. Chronic ethanol administration in mice causes migration of Candida albicans (C. albicans)-reactive Th17 cells from the intestine to the liver. The antifungal agent nystatin decreased C. albicans-specific Th17 cells in the liver and reduced ethanol-induced liver disease in mice. Transgenic mice expressing T cell receptors (TCRs) reactive to Candida antigens developed more severe ethanol-induced liver disease than transgene-negative littermates. Adoptively transferring Candida-specific TCR transgenic T cells or polyclonal C. albicans-primed T cells exacerbated ethanol-induced liver disease in wild-type mice. Interleukin-17 (IL-17) receptor A signaling in Kupffer cells was required for the effects of polyclonal C. albicans-primed T cells. Our findings indicate that ethanol increases C. albicans-specific Th17 cells, which contribute to alcohol-associated liver disease.

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Long Intergenic Noncoding RNA MIAT Contributes to Human Th17 Cell Differentiation

Project description:T helper 17 (Th17) cells protect against fungal and bacterial infections and are implicated in autoimmunity. Several long intergenic noncoding RNAs (lincRNA) are induced during Th17 differentiation, however, their contribution to Th17 differentiation is poorly understood. We discovered a lincRNA myocardial infarction associated transcript (MIAT) to be upregulated early after induction of human Th17 cell differentiation along with an increase in the chromatin accessibility at the gene locus. RNA-seq analysis identified genes implicated in Th17 differentiation and functions as MIAT targets. Our data suggests that MIAT contributes to human Th17 differentiation by upregulating several genes implicated in Th17 differentiation.

2022-05-25 | GSE183664 | GEO

Mouse Th17 T cells, IL-23 stimulated

Project description:Interleukin 23 (IL-23) triggers pathogenic features in pro-inflammatory, IL-17-secreting T cells (Th17 and Tγδ17) that play a key role in the development of inflammatory diseases. However, the IL-23 signaling cascade remains largely undefined. Here we used quantitative phosphoproteomics to characterize IL-23 signaling in primary murine Th17 cells. We quantified 6,888 phosphorylation sites in Th17 cells, and found 168 phosphorylations regulated upom IL-23 stimulation. IL-23 increased the phosphorylation of the myosin regulatory light chain (RLC), an actomyosin contractibility marker, in Th17 and Tγδ cells. IL-23-induced RLC phosphorylation required JAK2 and ROCK catalytic activity, and the study of the IL-23/ROCK axis revealed an unexpected role of IL-23 in the migration of Tγδ17 and Th17 cells. Moreover, pharmacological inhibition of ROCK reduced Tγδ17 recruitment to inflamed skin upon challenge with inflammatory agent Imiquimod. This work: i) provides new insights into phosphorylation networks that control Th17 cells, ii) widely expands the current knowledge on IL-23 signaling, and iii) contributes to the increasing list of immune cells subsets characterized by global phosphoproteomic approaches.

2020-03-25 | PXD016633 | Pride

Chromatin accessibility contributes to Candida albicans adaptation to echinocandins

Project description:Chromatin accessibility contributes to Candida albicans adaptation to echinocandins

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Candida albicans-specific Th17 cell-mediated response contributes to alcohol-associated liver disease

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

2023-02-16 | GSE215931 | GEO