Card9 and MyD88 differentially regulate Th17 immunity to the commensal yeast Malassezia in the murine skin
Open accessAbstract
The fungal community of the skin microbiome is dominated by a single genus, Malassezia. Besides its symbiotic lifestyle at the host interface, this commensal yeast has also been associated with diverse inflammatory skin diseases in humans and pet animals. Stable colonization is maintained by antifungal type 17 immunity. The mechanisms driving Th17 responses to Malassezia remain, however, unclear. Here, we show that the C-type lectin receptors Mincle, Dectin-1, and Dectin-2 recognize conserved patterns in the cell wall of Malassezia and induce dendritic cell activation in vitro, while only Dectin-2 is required for Th17 activation during experimental skin colonization in vivo. In contrast, Toll-like receptor recognition was redundant in this context. Instead, inflammatory IL-1 family cytokines signaling via MyD88 were also implicated in Th17 activation in a T cell-intrinsic manner. Taken together, we characterized the pathways contributing to protective immunity against the most abundant member of the skin mycobiome. This knowledge contributes to the understanding of barrier immunity and its regulation by commensals and is relevant considering how aberrant immune responses are associated with severe skin pathologies.
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A deficiency in the CLR adaptor Card9 does not affect C. auris control in the skin, unlike its requirement for induction of Th17 cells during cutaneous Malassezia infection.
“In contrast to C. albicans, a deficiency in the CLR adaptor Card9, required for the induction of Th17 cells during cutaneous Malassezia infection [10,101,102], did not affect C. auris control in the skin [3].”
From Host–Candida auris interactions in the skin (2026) · cites this paper as [101]
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Host–Candida auris interactions in the skin
Thangamani, S., Balakumar, A., Datta, A., Bryak, G., & Lionakis, M. S. (2026) · PLOS Pathogens · doi:10.1371/journal.ppat.1014075 · Cited by 3 · see citing works
- Authors
- Tuor, M., Stappers, M. H. T., Desgardin, A., Ruchti, F., Sparber, F., Orr, S. J., Gow, N. A. R., & LeibundGut-Landmann, S.
- Affiliations
- University of Zurich (CH)
- University of Exeter (GB)
- Queen's University Belfast (GB)
- ORCID
- Venue
- Mucosal Immunology
- Publisher
- Elsevier BV
- Published
- 2025-02
- Volume
- 18
- Issue
- 1
- Pages
- 205-219
- ISSN
- 1933-0219 (ISSN-L)
- OpenAlex
- W4404634209
- Cited by
- 10
- References
- 8
- Citations by year
- 2026: 7 · 2025: 3
- FWCI
- 1.67
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Mucosal Immunology (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Research Portal (Queen's University Belfast) (publishedVersion, cc-by)
- Funders
- UK Research and Innovation Medical Research Council (MR/N006364/2, MR/M026663/2)
- Swiss National Science Foundation (310030_189255)
- NIH Library (1R21-AI168672-01A1)
- NIHR Leicester Biomedical Research Centre
- Wellcome Trust (101873, 215599, 200208, 224323)
- NIHR Imperial Biomedical Research Centre
- National Institute for Health and Care Research
- Universität Zürich
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
- Health Sciences › Medicine › Epidemiology › Nail Diseases and Treatments
- Keywords
- Malassezia, Th17 response, skin mycobiome, commensal yeast, MyD88, CARD9, Dectin-2, Dectin-1, Mincle, C-type lectin receptors, dendritic cell activation, IL-1 signaling, skin colonization, barrier immunity, fungal cell wall recognition, inflammatory skin diseases
- MeSH terms
- Dectin-1, Animals, Cells, Cultured, Dendritic Cells, Dermatomycoses, Humans, Lymphocyte Activation, Malassezia, Membrane Proteins, Mice, Inbred C57BL, Skin, Symbiosis, Signal Transduction, Cytokines, Mice, Knockout, Lectins, C-Type, Mice, CARD Signaling Adaptor Proteins, Myeloid Differentiation Factor 88, Th17 Cells
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