The DOI matches its Crossref record; 129 of the 129 references it cites were found in a registry or an index.
IL-17–Mediated Immunity to the Opportunistic Fungal Pathogen Candida albicans
Open accessAbstract
IL-17 (IL-17A) has emerged as a key mediator of protection against extracellular microbes, but this cytokine also drives pathology in various autoimmune diseases. Overwhelming data in both humans and mice reveal a clear and surprisingly specific role for IL-17 in protection against the fungus Candida albicans, a commensal microbe of the human oral cavity, gastrointestinal tract, and reproductive mucosa. The IL-17 pathway regulates antifungal immunity through upregulation of proinflammatory cytokines, including IL-6, neutrophil-recruiting chemokines (e.g., CXCL1 and CXCL5), and antimicrobial peptides (e.g., defensins), which act in concert to limit fungal overgrowth. This review focuses on diseases caused by C. albicans, the role of IL-17–mediated immunity in candidiasis, and the implications for clinical therapies for both autoimmune conditions and fungal infections.
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“The PRRs in the myeloid cells facilitate fungal recognition in the host [24, 38]”
From Single-cell transcriptomics unveils skin cell specific antifungal immune responses and IL-1Ra- IL-1R immune evasion strategies of emerging fungal pathogen Candida auris (2024) · cites this paper as [38]
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Cites
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Hidden Killers: Human Fungal Infections
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β-Defensins: Linking Innate and Adaptive Immunity Through Dendritic and T Cell CCR6
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Innate IL-17-producing cells: the sentinels of the immune system
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The IL-23-IL-17 immune axis: from mechanisms to therapeutic testing
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Self-citationPneumocystis Pneumonia—Los Angeles
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Metadata
- Authors
- Conti, H. R., & Gaffen, S. L.
- Affiliations
- University of Pittsburgh (US)
- Corresponding author
- Gaffen, Sarah L
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2015-08-01
- Volume
- 195
- Issue
- 3
- Pages
- 780-788
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- PMC
- PMC4507294
- OpenAlex
- W1912289137
- Cited by
- 301
- References
- 129
- Citations by year
- 2026: 28 · 2025: 29 · 2024: 20 · 2023: 19 · 2022: 35 · 2021: 26 · 2020: 35 · 2019: 28 · 2018: 34 · 2017: 22 · 2016: 22 · 2015: 2
- FWCI
- 4.05
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (5r37de022550-12, DE022550)
- National Institute of Allergy and Infectious Diseases (R01AI107825, AI107825)
- National Institute of Dental and Craniofacial Research (R37-DE022550, F32DE023293, R01DE022550, R01DE023815, DE022550)
- Topics
- Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
- Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Keywords
- IL-17, IL-17A, Candida albicans, antifungal immunity, candidiasis, opportunistic fungal infection, neutrophil recruitment, CXCL1, CXCL5, antimicrobial peptides, defensins, interleukin-6, inflammatory cytokines, autoimmune disease, fungal overgrowth
- MeSH terms
- Animals, Candida albicans, Candidiasis, Humans, Neutrophils, Opportunistic Infections, Signal Transduction, Interleukin-6, Interleukin-17, Neutrophil Infiltration, Defensins, Receptors, Pattern Recognition, Mice, Receptors, Interleukin-17, Chemokine CXCL1, Chemokine CXCL5
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