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T cell AHR activity tunes the Gut Microenvironment to Sustain Autoimmunity.

ABSTRACT: T cell AHR activity tunes the Gut Microenvironment to Sustain Autoimmunity.

PROVIDER: PRJNA824497 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18677500_1.fastq.gz	Fastqsanger.gz
	SRR18677500_2.fastq.gz	Fastqsanger.gz
	SRR18677501_1.fastq.gz	Fastqsanger.gz
	SRR18677501_2.fastq.gz	Fastqsanger.gz
	SRR18677502_1.fastq.gz	Fastqsanger.gz

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T cell AHR activity tunes the Gut Microenvironment to Sustain Autoimmunity [sephouse_cecum]

Project description:T cell AHR activity tunes the Gut Microenvironment to Sustain Autoimmunity [sephouse_cecum]

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T cell AHR activity tunes the Gut Microenvironment to Sustain Autoimmunity [sephouse_feces]

Project description:T cell AHR activity tunes the Gut Microenvironment to Sustain Autoimmunity [sephouse_feces]

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T cell AHR activity tunes the Gut Microenvironment to Sustain Autoimmunity [cohouse_feces]

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T cell AHR activity tunes the Gut Microenvironment to Sustain Autoimmunity [sephouse_feces]

Project description:The contribution of the environment and, in particular, the gut flora to multiple sclerosis (MS) etiology is well documented but not well understood. The aryl hydrocarbon receptor (AHR) binds numerous molecules present in the environment and is a therapeutic target for MS: however, its precise function in T lymphocytes, the orchestrators of MS, has not been described. Here, we show that CD4 specific Ahr knockout drives recovery in an animal model of MS driven by a decrease in T cell fitness. At the mechanistic level, we show that the absence of AHR changes the gut microenvironment composition to generate metabolites, such as bile salts and short chain fatty acids, that impact T cell viability. Our study demonstrates a newly emerging role for AHR in mediating the interdependence between T lymphocytes and the microbiota while identifying new potential molecular targets for the treatment of MS and other autoimmune diseases.

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T cell AHR activity tunes the Gut Microenvironment to Sustain Autoimmunity [sephouse_cecum]

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T cell AHR activity tunes the Gut Microenvironment to Sustain Autoimmunity [cohouse_feces]

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T cell AHR activity tunes the Gut Microenvironment to Sustain Autoimmunity.

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

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Tissue-resident memory CD4+ T cells sustain chronic CNS autoimmunity

Project description:Tissue-resident memory CD4+ T cells sustain chronic CNS autoimmunity

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AhR interactome in early embryonic development

Project description:The transcriptional program of early embryonic development is tightly regulated by a set of well-defined transcription factors that suppress premature expression of differentiation genes and sustain the pluripotent identity. It is generally accepted that this program can be perturbed by environmental factors such as chemical pollutants, however the precise molecular mechanisms remain unknown. The Aryl Hydrocarbon Receptor (AHR) is a widely expressed nuclear receptor that senses environmental stimuli and modulates target gene expression. Here, we show that ectopic activation of AHR during early differentiation disrupts the differentiation program via the chromatin remodeling complex NuRD. The activated AHR/NuRD complex altered the expression of differentiation-specific genes that control the first two developmental decisions without affecting the pluripotency program. These findings identify a novel mechanism that allows environmental stimuli to disrupt embryonic development through AHR signaling.

2018-02-26 | PXD006089 | Pride

The activity of the aryl hydrocarbon receptor in T cells tunes the gut microenvironment to sustain autoimmunity and neuroinflammation.

Project description:Multiple sclerosis (MS) is a T cell-driven autoimmune disease that attacks the myelin of the central nervous system (CNS) and currently has no cure. MS etiology is linked to both the gut flora and external environmental factors but this connection is not well understood. One immune system regulator responsive to nonpathogenic external stimuli is the aryl hydrocarbon receptor (AHR). The AHR, which binds diverse molecules present in the environment in barrier tissues, is a therapeutic target for MS. However, AHR's precise function in T lymphocytes, the orchestrators of MS, has not been described. Here, we show that in a mouse model of MS, T cell-specific Ahr knockout leads to recovery driven by a decrease in T cell fitness. At the mechanistic level, we demonstrate that the absence of AHR changes the gut microenvironment composition to generate metabolites that impact T cell viability, such as bile salts and short chain fatty acids. Our study demonstrates a newly emerging role for AHR in mediating the interdependence between T lymphocytes and the microbiota, while simultaneously identifying new potential molecular targets for the treatment of MS and other autoimmune diseases.

| S-EPMC9928083 | biostudies-literature

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