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The skin commensal yeast malassezia triggers a type 17 response that coordinates anti-fungal immunity and exacerbates skin inflammation


Sparber, Florian; De Gregorio, Corinne; Steckholzer, Simone; Ferreira, Filipa M; Dolowschiak, Tamas; Ruchti, Fiorella; Kirchner, Florian R; Mertens, Sarah; Prinz, Immo; Joller, Nicole; Buch, Thorsten; Glatz, Martin; Sallusto, Federica; LeibundGut-Landmann, Salomé (2019). The skin commensal yeast malassezia triggers a type 17 response that coordinates anti-fungal immunity and exacerbates skin inflammation. Cell Host & Microbe, 25(3):389-403.e6.

Abstract

Commensal fungi of the mammalian skin, such as those of the genus Malassezia, are associated with atopic dermatitis and other common inflammatory skin disorders. Understanding of the causative relationship between fungal commensalism and disease manifestation remains incomplete. By developing a murine epicutaneous infection model, we found Malassezia spp. selectively induce IL-17 and related cytokines. This response is key in preventing fungal overgrowth on the skin, as disruption of the IL-23-IL-17 axis compromises Malassezia-specific cutaneous immunity. Under conditions of impaired skin integrity, mimicking a hallmark of atopic dermatitis, the presence of Malassezia dramatically aggravates cutaneous inflammation, which again was IL-23 and IL-17 dependent. Consistently, we found a CCR6+ Th17 subset of memory T cells to be Malassezia specific in both healthy individuals and atopic dermatitis patients, whereby the latter showed enhanced frequency of these cells. Thus, the Malassezia-induced type 17 response is pivotal in orchestrating antifungal immunity and in actively promoting skin inflammation

Abstract

Commensal fungi of the mammalian skin, such as those of the genus Malassezia, are associated with atopic dermatitis and other common inflammatory skin disorders. Understanding of the causative relationship between fungal commensalism and disease manifestation remains incomplete. By developing a murine epicutaneous infection model, we found Malassezia spp. selectively induce IL-17 and related cytokines. This response is key in preventing fungal overgrowth on the skin, as disruption of the IL-23-IL-17 axis compromises Malassezia-specific cutaneous immunity. Under conditions of impaired skin integrity, mimicking a hallmark of atopic dermatitis, the presence of Malassezia dramatically aggravates cutaneous inflammation, which again was IL-23 and IL-17 dependent. Consistently, we found a CCR6+ Th17 subset of memory T cells to be Malassezia specific in both healthy individuals and atopic dermatitis patients, whereby the latter showed enhanced frequency of these cells. Thus, the Malassezia-induced type 17 response is pivotal in orchestrating antifungal immunity and in actively promoting skin inflammation

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Dermatology Clinic
05 Vetsuisse Faculty > Institute of Laboratory Animal Science
05 Vetsuisse Faculty > Institute of Virology
04 Faculty of Medicine > Institute of Experimental Immunology
Dewey Decimal Classification:570 Life sciences; biology
Uncontrolled Keywords:Microbiology, Parasitology, Virology, Malassezia; Th17; atopic dermatitis; fungal commensalism; inflammation; interleukin-17; interleukin-23; skin immunity; skin microbiota; γδ T cells
Language:English
Date:1 March 2019
Deposited On:22 Mar 2019 11:06
Last Modified:22 Mar 2019 12:07
Publisher:Cell Press (Elsevier)
ISSN:1931-3128
OA Status:Closed
Free access at:Publisher DOI. An embargo period may apply.
Publisher DOI:https://doi.org/10.1016/j.chom.2019.02.002
Project Information:
  • : FunderH2020
  • : Grant ID677200
  • : Project TitleImmune Regulation - How Infection History Shapes the Immune System: Pathogen-induced Changes in Regulatory T Cells
  • : FunderFP7
  • : Grant ID323183
  • : Project TitlePREDICT - Dissecting the human T cell response to pathogens, allergens, and self-antigens
  • : FunderSNSF
  • : Grant IDPP00P3_150663
  • : Project TitleImmune Regulation through Infection History

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