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 language | English |
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Pages (from-to) | 389-403.e6 |
Journal | Cell Host and Microbe |
Volume | 25 |
Issue number | 3 |
DOIs | |
State | Published - 13 Mar 2019 |
Externally published | Yes |
Keywords
- Malassezia
- Th17
- atopic dermatitis
- fungal commensalism
- inflammation
- interleukin-17
- interleukin-23
- skin immunity
- skin microbiota
- γδ T cells