Immunity to commensal skin fungi promotes psoriasiform skin inflammation
Open accessAbstract
Significance: Tissues exposed to the environment are sites of exposure to symbiotic microbes including fungi that are continuously sensed by the immune system. Here, we show that immunity to commensal skin fungi can significantly aggravate tissue inflammation. Enhanced pathology caused by fungi preexposure depends on lymphocytes able to produce the cytokine IL-17 and the formation of extracellular traps by neutrophils. We also found that fungal exposure prior to experimental modeling of psoriasis recapitulates features of the transcriptional landscape of human lesional psoriatic skin. Together, our results propose that recall responses directed to skin fungi can directly promote skin inflammation and that exploration of tissue inflammation should be assessed in the context of recall responses to the microbiota.
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IL-17+ T cell responses can promote tissue inflammatory diseases in predisposed hosts.
“It was suggested that while IL-17+ T cell responses are important in controlling commensal fungi or fungal pathogens, they can promote tissue inflammatory diseases in predisposed hosts.41,42,43”
From Skin-resident T cells play an important role in controlling skin colonization of Candidozyma (Candida) auris (2026) · cites this paper as [43]
IL-17+ T cell responses are important in controlling commensal fungi or fungal pathogens.
“It was suggested that while IL-17+ T cell responses are important in controlling commensal fungi or fungal pathogens, they can promote tissue inflammatory diseases in predisposed hosts.41,42,43”
From Skin-resident T cells play an important role in controlling skin colonization of Candidozyma (Candida) auris (2026) · cites this paper as [43]
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Merrill, E. D., Prudent, V., Basso, P., Rapp, E., Moghadam, P., Rodriguez, A., Hung, E., Hurabielle, C., Cheng, J., Cho, R. J., et al. (2026) · Science · doi:10.1126/science.adu6688 · Cited by 5 · see citing works
Self-citationThe emerging fungal pathogen <i>Candida auris</i> induces IFNγ to colonize mammalian hair follicles
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Self-citationXie, J., Yan, L., Kadosh, D., & Xiong, N. (2026) · iScience · doi:10.1016/j.isci.2026.115862 · Cited by 1 · see citing works
- Authors
- Hurabielle, C., Link, V. M., Bouladoux, N., Han, S.-J., Merrill, E. D., Lightfoot, Y. L., Seto, N., Bleck, C. K. E., Smelkinson, M., Harrison, O. J., Linehan, J. L., Tamoutounour, S., Lionakis, M. S., Kaplan, M. J., Nakajima, S., & Belkaid, Y.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Nakajima, Saeko
- Belkaid, Yasmine
- ORCID
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2020-06-29
- Volume
- 117
- Issue
- 28
- Pages
- 16465-16474
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC7368261
- OpenAlex
- W3039428566
- Cited by
- 97
- References
- 8
- Citations by year
- 2026: 7 · 2025: 11 · 2024: 15 · 2023: 14 · 2022: 22 · 2021: 19 · 2020: 9
- FWCI
- 5.60
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Division of Intramural Research, National Institute of Allergy and Infectious Diseases (ZIA-AI001115, ZIA-AI001132, ZIA-AI001175)
- HHS | NIH | National Institute of Arthritis and Musculoskeletal and Skin Diseases (ZIA-AR041199)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- psoriasis, recall immune response, Th17 cells, neutrophil extracellular traps, skin inflammation
- MeSH terms
- Animals, Arthrodermataceae, Female, Humans, Immunity, Male, Mice, Inbred C57BL, Psoriasis, Skin, Symbiosis, Mice, Th17 Cells, Microbiota, Extracellular Traps
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