S9.5c Malassezia-host interactions and the Il-23/17 axis

S9.5 MALASSEZIA: PATHOGENESIS AND DISEASE, SEPTEMBER 23, 2022, 4:45 PM - 6:15 PM: : The mycobiome of the skin is dominated by a single fungal genus, Malassezia. While Malassezia normally exists as a commensal without inflicting disease, the fungus has also been associated with numerous skin disorders ranging from mild conditions such as dandruff or pityriasis versicolor to severe chronic pathologies such as seborrheic or atopic dermatitis. Maintaining stable colonization and preventing pathogenicity of Malassezia is key for skin homeostasis. Our understanding of the fungal factors and host mechanisms that, through mutual interactions, promote Malassezia commensalism in healthy skin remains incomplete. From studies in humans and mice, we learned that homeostatic immunity against Malassezia is characterized by IL-17-producing T cells, including Th17 and γδT17 cells. Recent endeavors start to unravel the cellular and molecular pathways responsible for driving the protective antifungal response in the skin. While Malassezia-responsive T cells are non-inflammatory and host-beneficial, they can bear pathogenic potential and thereby be involved in the pathogenesis of inflammatory and allergic skin conditions, as preclinical studies suggest. During my lecture, I will report on recent findings from my lab regarding the role and regulation of the IL-23/IL-17 axis in response to Malassezia under normal and diseased skin conditions.