IL-22 defines a novel immune pathway of antifungal resistance
Open accessAbstract
The role of IL-17 and Th17 cells in immunity vs. pathology associated with the human commensal Candida albicans remains controversial. Both positive and negative effects on immune resistance have been attributed to IL-17/Th17 in experimental candidiasis. In this study, we provide evidence that IL-22, which is also produced by Th17 cells, has a critical, first-line defense in candidiasis by controlling the growth of infecting yeasts as well as by contributing to the host's epithelial integrity in the absence of acquired Th1-type immunity. The two pathways are reciprocally regulated, and IL-22 is upregulated under Th1 deficiency conditions and vice versa. Whereas both IL-17A and F are dispensable for antifungal resistance, IL-22 mediates protection in IL-17RA-deficient mice, in which IL-17A contributes to disease susceptibility. Thus, our findings suggest that protective immunity to candidiasis is made up of a staged response involving an early, IL-22-dominated response followed by Th1/Treg reactivity that will prevent fungal dissemination and supply memory.
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TH17 cells secrete IL-17, IL-21 and IL-22 and are important for the control of fungal infection.
“T H 17 cells secrete IL-17, IL-21 and IL-22 and are important for the control of fungal infection (De Luca et al., 2010).”
From Iron in infection and immunity (2020) · cites this paper as De Luca et al., 2010
The Introduction says Th17 cells produce IL-22, and the paper’s conclusion describes an important role for the Th17 pathway in antifungal resistance. Our copy does not say that Th17 cells secrete IL-21. It also distinguishes the protective effect of IL-22 from IL-17A, which it reports can adversely affect resistance in some Candida infection settings. (LLM, conf=0.88)
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References 59 · Cited by 265
- Authors
- De Luca, A., Zelante, T., D'Angelo, C., Zagarella, S., Fallarino, F., Spreca, A., Iannitti, R. G., Bonifazi, P., Renauld, J.-C., Bistoni, F., Puccetti, P., & Romani, L.
- Affiliations
- University of Perugia (IT)
- Ludwig Cancer Research (BE)
- Corresponding author
- Romani, L
- Venue
- Mucosal Immunology
- Publisher
- Elsevier BV
- Published
- 2010-07
- Volume
- 3
- Issue
- 4
- Pages
- 361-373
- ISSN
- 1933-0219 (ISSN-L)
- OpenAlex
- W2117613919
- Cited by
- 265
- References
- 59
- Citations by year
- 2026: 2 · 2025: 8 · 2024: 13 · 2023: 11 · 2022: 14 · 2021: 11 · 2020: 15 · 2019: 9 · 2018: 11 · 2017: 22 · 2016: 20 · 2015: 20 · 2014: 33 · 2013: 19 · 2012: 21
- FWCI
- 15.70
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Mucosal Immunology (publishedVersion)
- PubMed (publishedVersion)
- Digital Access to Libraries (submittedVersion)
- INFM-OAR (INFN Catania) (submittedVersion, other-oa)
- Funders
- European Commission (242220)
- Topics
- Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- IL-22, IL-17, Th17 cells, Candida albicans, experimental candidiasis, antifungal immunity, IL-17RA, Th1 response, regulatory T cells, epithelial barrier integrity, fungal dispersal, commensal fungi
- MeSH terms
- Interleukin-22, Animals, Candida albicans, Candidiasis, Cells, Cultured, Humans, Interleukins, Intestinal Mucosa, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Knockout, Th1 Cells, Th2 Cells, Immunity, Mucosal, Interleukin-17, Models, Animal, Cell Growth Processes, Mice, Receptors, Interleukin-17
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