ArticleJournal of leukocyte biology2016
Antibody blockade of IL-17 family cytokines in immunity to acute murine oral mucosal candidiasis.
Article in Journal of leukocyte biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 38 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
38 citing papers in PubMed, 62 citations in OpenAlex.
- γδ T cells and cancer.The Journal of clinical investigation · 2026Review
- An IL-1, IL-17, and IL-22 cytokine circuit controls vulvovaginal candidiasis independently of estrogen.PLoS pathogens · 2026Article
- Abundant Yet Aberrant T Helper Cell Responses to Candida albicans Underlie Mucosal Candidiasis in Humans and Mice.European journal of immunology · 2025Article
- Real-world effectiveness and safety of bimekizumab in Japanese patients with psoriasis: A single-center retrospective study.The Journal of dermatology · 2024Article
- IκBζ is an essential mediator of immunity to oropharyngeal candidiasis.Cell host & microbe · 2023Article
- The IL-17 family in diseases: from bench to bedside.Signal transduction and targeted therapy · 2023Review
- Friend or Foe - Tc17 cell generation and current evidence for their importance in human disease.Discovery immunology · 2023Review
- The IL-17 pathway as a target in giant cell arteritis.Frontiers in immunology · 2023Review
- A gut-oral microbiome-driven axis controls oropharyngeal candidiasis through retinoic acid.JCI insight · 2022Article
- Epidermal clearance of Candida albicans is mediated by IL-17 but independent of fungal innate immune receptors.International immunology · 2022Article
- Divergent functions of IL-17-family cytokines in DSS colitis: Insights from a naturally-occurring human mutation in IL-17F.Cytokine · 2021Article
- Crosstalk between the oral microbiota, mucosal immunity, and the epithelial barrier regulates oral mucosal disease pathogenesis.Mucosal immunology · 2021Review
- Infections in the monogenic autoimmune syndrome APECED.Current opinion in immunology · 2021Review
- Bimekizumab for the Treatment of Psoriasis.Drugs · 2021Review
- T Cell-Intrinsic Interferon Regulatory Factor 1 Expression Suppresses Differentiation of CD4Journal of virology · 2021Article
- Response to Comments on "Aberrant type 1 immunity drives susceptibility to mucosal fungal infections".Science (New York, N.Y.) · 2021Article
- Interference with the expression of S1PR1 or STAT3 attenuates valvular damage due to rheumatic heart disease.International journal of molecular medicine · 2021Article
- The impact of the Fungus-Host-Microbiota interplay upon Candida albicans infections: current knowledge and new perspectives.FEMS microbiology reviews · 2021Review
- Aberrant type 1 immunity drives susceptibility to mucosal fungal infections.Science (New York, N.Y.) · 2021Article
- Review
Corrections and comments
- Erratum issuedErratum.2017
Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Antibodies targeting IL-17A or its receptor, IL-17RA, are approved to treat psoriasis and are being evaluated for other autoimmune conditions. Conversely, IL-17 signaling is critical for immunity to opportunistic mucosal infections caused by the commensal fungus Candida albicans, as mice and humans lacking the IL-17R experience chronic mucosal candidiasis. IL-17A, IL-17F, and IL-17AF bind the IL-17RA-IL-17RC heterodimeric complex and deliver qualitatively similar signals through the adaptor Act1. Here, we used a mouse model of acute oropharyngeal candidiasis to assess the impact of blocking IL-17 family cytokines compared with specific IL-17 cytokine gene knockout mice. Anti-IL-17A antibodies, which neutralize IL-17A and IL-17AF, caused elevated oral fungal loads, whereas anti-IL-17AF and anti-IL-17F antibodies did not. Notably, there was a cooperative effect of blocking IL-17A, IL-17AF, and IL-17F together. Termination of anti-IL-17A treatment was associated with rapid C. albicans clearance. IL-17F-deficient mice were fully resistant to oropharyngeal candidiasis, consistent with antibody blockade. However, IL-17A-deficient mice had lower fungal burdens than anti-IL-17A-treated mice. Act1-deficient mice were much more susceptible to oropharyngeal candidiasis than anti-IL-17A antibody-treated mice, yet anti-IL-17A and anti-IL-17RA treatment caused equivalent susceptibilities. Based on microarray analyses of the oral mucosa during infection, only a limited number of genes were associated with oropharyngeal candidiasis susceptibility. In sum, we conclude that IL-17A is the main cytokine mediator of immunity in murine oropharyngeal candidiasis, but a cooperative relationship among IL-17A, IL-17AF, and IL-17F exists in vivo. Susceptibility displays the following hierarchy: IL-17RA- or Act1-deficiency > anti-IL-17A + anti-IL-17F antibodies > anti-IL-17A or anti-IL-17RA antibodies > IL-17A deficiency.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.