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

• DOI: 10.1016/j.mucimm.2024.11.004
• Publication Date: 2024-11-22T16:40:06Z
• Authors: Meret Tuor; Mark H.T. Stappers; Alice Desgardin; Fiorella Ruchti; Florian Sparber; Selinda J. Orr; Neil A.R. Gow; Salomé LeibundGut...
• Keywords: Malassezia

The fungal community of the skin microbiome is dominated by a single genus, Malassezia. Besides its symbiotic lifestyle at host interface, this commensal yeast has also been associated with diverse inflammatory diseases in humans and pet animals. Stable colonization maintained antifungal type 17 immunity. mechanisms driving Th17 responses to Malassezia remain, however, unclear. Here, we show that C-type lectin receptors Mincle, Dectin-1, Dectin-2 recognize conserved patterns cell wall induce dendritic activation vitro, while only required for during experimental vivo. In contrast, Toll-like receptor recognition was redundant context. Instead, IL-1 family cytokines signaling via MyD88 were implicated T cell-intrinsic manner. Taken together, characterized pathways contributing protective immunity against most abundant member mycobiome. This knowledge contributes understanding barrier regulation commensals relevant considering how aberrant immune are severe pathologies.