The Skin Commensal Yeast Malassezia Triggers a Type 17 Response that Coordinates Anti-fungal Immunity and Exacerbates Skin Inflammation

Florian Sparber, Corinne De Gregorio, Simone Steckholzer, Filipa M. Ferreira, Tamas Dolowschiak, Fiorella Ruchti, Florian R. Kirchner, Sarah Mertens, Immo Prinz, Nicole Joller, Thorsten Buch, Martin Glatz, Federica Sallusto, Salomé LeibundGut-Landmann

Research output: Contribution to journalArticlepeer-review

181 Scopus citations

Abstract

The skin commensal yeast Malassezia is associated with common skin disorders like atopic dermatitis, but how the mammalian host responds to Malassezia remains unclear. Using an epicutaneous infection model in mice, Sparber et al. demonstrate that the IL-23-IL-17 pathway controls fungal colonization and also drives Malassezia-induced inflammation in atopy-like skin.

Original languageEnglish
Pages (from-to)389-403.e6
JournalCell Host and Microbe
Volume25
Issue number3
DOIs
StatePublished - 13 Mar 2019
Externally publishedYes

Keywords

  • Malassezia
  • Th17
  • atopic dermatitis
  • fungal commensalism
  • inflammation
  • interleukin-17
  • interleukin-23
  • skin immunity
  • skin microbiota
  • γδ T cells

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