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ABSTRACT: Innate type 2 immunity controls hair follicle commensalism by Demodex mites

PROVIDER: PRJNA861245 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20462420_1.fastq.gz	Fastqsanger.gz
	SRR20462420_2.fastq.gz	Fastqsanger.gz
	SRR20462421_1.fastq.gz	Fastqsanger.gz
	SRR20462421_2.fastq.gz	Fastqsanger.gz
	SRR20462422_1.fastq.gz	Fastqsanger.gz

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Innate type 2 immunity controls hair follicle commensalism by Demodex mites

Project description:Innate type 2 immunity controls hair follicle commensalism by Demodex mites

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Innate type 2 immunity controls hair follicle commensalism by Demodex mites [IL-4, IL-13]

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Innate type 2 immunity controls hair follicle commensalism by Demodex mites [2021]

Project description:Demodex mites are obligate commensal parasites of hair follicles (HF) in mammals. Normally asymptomatic, inflammatory outgrowth of mites can accompany malnutrition, immune dysfunction and aging, but mechanisms restricting Demodex outgrowth and pathogenesis are not defined. Here, we show that control over mite HF colonization of mice requires ILC2s, IL-13, and its receptor IL-4Ra, but not IL-4 or the adaptive immune system. Epithelial HF-associated ILC2s elaborate IL-13 that attenuates HF and epithelial cell proliferation at anagen onset; in their absence, Demodex colonization leads to increased epithelial proliferation and replacement of gene programs for repair by aberrant inflammatory programs leading to loss of barrier function and premature HF exhaustion over time. Humans with rhinophymatous acne rosacea, a nasal inflammatory condition associated with a high burden of Demodex, had increased HF inflammatory cells with decreased type 2 cytokines, consistent with the inverse relationship seen in mice. Our studies uncover a critical role for skin ILC2s and IL-13, which comprise an immune checkpoint necessary to sustain cutaneous integrity and restrict pathologic infestation by colonizing HF mites.

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Project description:Tight immune defense against environment and a unique ability of self-repair are the hallmarks of epithelia. Here we show that innate immunity Toll like receptor 2 (TLR2) coordinates these key functions thereby promoting hair growth and tissue regeneration. TLR2 is enriched in hair follicle stem cells (HFSCs) and its levels change in hair cycle and skin disorders. The lack of TLR2 in HFSCs diminishes activation and proliferation of HFSCs markedly prolonging the resting phase of hair cycle. Transcriptome profiling of HFSCs revealed that TLR2 regulates main hair regeneration pathways. TLR2 deletion upregulates inhibitory BMP7 signaling, while the blockade by Noggin restores deficient HFSCs proliferation in the absence of TLR2. In injury model TLR2 is required for both, tissue and hair regeneration. While endothelial TLR2 drives wound revascularization and closure, HFSC TLR2 controls hair regrowth. Endogenous TLR2 ligand produced in hair follicles promotes hair regeneration and growth via HFSC TLR2. Together, HFSC TLR2 drives stem cell proliferation, hair cycle and regeneration.

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