Card9 and MyD88 differentially regulate Th17 immunity to the commensal yeast Malassezia in the murine skin.

Autor:	Tuor M; Section of Immunology, Vetsuisse Faculty and Institute of Experimental Immunology, University of Zürich, 8057 Zurich, Switzerland., Stappers MHT; Medical Research Council Centre for Medical Mycology at the University of Exeter, Department of Biosciences, Faculty of Health and Life Sciences, Geoffrey Pope Building, Stocker Road, Exeter EX4 4QD, UK., Desgardin A; Section of Immunology, Vetsuisse Faculty and Institute of Experimental Immunology, University of Zürich, 8057 Zurich, Switzerland., Ruchti F; Section of Immunology, Vetsuisse Faculty and Institute of Experimental Immunology, University of Zürich, 8057 Zurich, Switzerland., Sparber F; Section of Immunology, Vetsuisse Faculty and Institute of Experimental Immunology, University of Zürich, 8057 Zurich, Switzerland., Orr SJ; Wellcome-Wolfson Institute for Experimental Medicine, School of Medicine, Dentistry and Biomedical Science, Queen's University Belfast, Belfast BT9 7BL, UK., Gow NAR; Medical Research Council Centre for Medical Mycology at the University of Exeter, Department of Biosciences, Faculty of Health and Life Sciences, Geoffrey Pope Building, Stocker Road, Exeter EX4 4QD, UK., LeibundGut-Landmann S; Section of Immunology, Vetsuisse Faculty and Institute of Experimental Immunology, University of Zürich, 8057 Zurich, Switzerland; Medical Research Council Centre for Medical Mycology at the University of Exeter, Department of Biosciences, Faculty of Health and Life Sciences, Geoffrey Pope Building, Stocker Road, Exeter EX4 4QD, UK. Electronic address: salome.leibundgut-landmann@uzh.ch.
Jazyk:	angličtina
Zdroj:	Mucosal immunology [Mucosal Immunol] 2024 Nov 22. Date of Electronic Publication: 2024 Nov 22.
DOI:	10.1016/j.mucimm.2024.11.004
Abstrakt:	The fungal community of the skin microbiome is dominated by a single genus, Malassezia. Besides its symbiotic lifestyle at the host interface, this commensal yeast has also been associated with diverse inflammatory skin diseases in humans and pet animals. Stable colonization is maintained by antifungal type 17 immunity. The mechanisms driving Th17 responses to Malassezia remain, however, unclear. Here, we show that the C-type lectin receptors Mincle, Dectin-1, and Dectin-2 recognize conserved patterns in the cell wall of Malassezia and induce dendritic cell activation in vitro, while only Dectin-2 is required for Th17 activation during experimental skin colonization in vivo. In contrast, Toll-like receptor recognition was redundant in this context. Instead, inflammatory IL-1 family cytokines signaling via MyD88 were also implicated in Th17 activation in a T cell-intrinsic manner. Taken together, we characterized the pathways contributing to protective immunity against the most abundant member of the skin mycobiome. This knowledge contributes to the understanding of barrier immunity and its regulation by commensals and is relevant considering how aberrant immune responses are associated with severe skin pathologies. Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. (Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.)
Databáze:	MEDLINE
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