Cited by 301Antifungal resistance and susceptibilityIL-33, ST2, and ILC PathwaysPsoriasis: Treatment and Pathogenesis

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IL-17–Mediated Immunity to the Opportunistic Fungal Pathogen Candida albicans

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Conti, Heather R, Gaffen, Sarah L·2015·The Journal of Immunology

DOI 10.4049/jimmunol.1500909PMC PMC4507294

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Abstract

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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Authors: Conti, H. R., & Gaffen, S. L.
Affiliations: University of Pittsburgh (US)
Corresponding author: Gaffen, Sarah L
ORCID: Conti, Heather R
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
DOI: 10.4049/jimmunol.1500909
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
Licence: academic.oup.com/pages/standard-publication-reuse-rights (vor)
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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IL-17–Mediated Immunity to the Opportunistic Fungal Pathogen Candida albicans

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