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Tet2 deficiency drives pathobiont translocation triggering Tc1 cell autoimmune hepatitis

ABSTRACT: Tet2 deficiency drives pathobiont translocation triggering Tc1 cell autoimmune hepatitis

PROVIDER: PRJNA831834 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18912911.fastq.gz	Fastqsanger.gz
	SRR18912912.fastq.gz	Fastqsanger.gz
	SRR18912913.fastq.gz	Fastqsanger.gz
	SRR18912914.fastq.gz	Fastqsanger.gz
	SRR18912915.fastq.gz	Fastqsanger.gz

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Tet2 deficiency drives pathobiont translocation triggering Tc1 cell autoimmune hepatitis

Project description:The triggers that drive interferon-g (IFNg)-producing CD8 T cell (Tc1 cell)-mediated autoimmune hepatitis (AIH) remain obscure. Here we show that lack of hematopoietic Tet methylcytosine dioxygenase 2 (Tet2), an epigenetic regulator associated with autoimmunity, results in the development of microbiota-dependent AIH-like pathology, accompanied by hepatic enrichment of aryl hydrocarbon receptor (AhR) ligand-producing pathobionts and rampant Tc1 cell immunity. We report that AIH-like disease development is dependent on both IFNg and AhR signaling, as blocking either reverts ongoing AIH-like pathology. Illustrating the critical role of AhR ligand-producing pathobionts in this condition, hepatic translocation of the AhR ligand indole-3-aldehyde (I3A)-releasing Lactobacillus reuteri is sufficient to trigger AIH-like pathology. Finally, we demonstrate that I3A is required for L. reuteri-induced Tc1 cell differentiation in vitro and AIH-like pathology in vivo, both of which are restrained by Tet2 within CD8 T cells. This AIH-disease model may contribute to the development of therapeutics to alleviate AIH.

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