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Adaptive immunity to retroelements promotes barrier integrity [bulk_DC_KC_LC]

ABSTRACT: Adaptive immunity to retroelements promotes barrier integrity [bulk_DC_KC_LC]

PROVIDER: PRJNA1107528 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28894000_1.fastq.gz	Fastqsanger.gz
	SRR28894000_2.fastq.gz	Fastqsanger.gz
	SRR28894001_1.fastq.gz	Fastqsanger.gz
	SRR28894001_2.fastq.gz	Fastqsanger.gz
	SRR28894002_1.fastq.gz	Fastqsanger.gz

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Adaptive immunity to retroelements promotes barrier integrity [bulk_DC_KC_LC]

Project description:The skin is the body’s largest and outermost barrier tissue. Whether environmental exposures reinforce barrier resilience remains poorly understood. Here, we show that xenobiotic-induced retroelement-specific immunity enhances tissue repair; more specifically, mild detergent exposure promotes the reactivation of defined retroelements, and retroelement-specific CD8+ responses, in a Langerhans cell-dependent manner. This discrete population of retroelement-specific CD8 T cells are recruited to the skin, where they develop as tissue-resident cells and are enriched for genes associated with wound repair. Upon injury, retroelement-specific CD8+ T cells significantly accelerate wound repair via IL-17A. Collectively, this work demonstrates that tonic environmental exposures promote the accumulation of tissue-resident retroelement-specific T cells that preemptively set the tissue for maximal resilience to barrier breaches.

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Project description:Maintenance of tissue integrity is a requirement of host survival. This mandate is of prime importance at barrier sites that are constitutively exposed to the environment. Here, we show that exposure of the skin to non-inflammatory xenobiotics promotes tissue repair; more specifically, mild detergent exposure promotes the reactivation of defined retroelements leading to the induction of retroelement-specific CD8+ T cells. These T cell responses are Langerhans cell dependent and establish tissue residency within the skin. Upon injury, retroelement-specific CD8+ T cells significantly accelerate wound repair via IL-17A. Collectively, this work demonstrates that tonic environmental exposures and associated adaptive responses to retroelements can be coopted to preemptively set the tissue for maximal resilience to injury.

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