ArticleBMC immunology2014
Defective IL-17- and IL-22-dependent mucosal host response to Candida albicans determines susceptibility to oral candidiasis in mice expressing the HIV-1 transgene.
Article in BMC immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Deciphering Candida's Genomic Influence on Oral Squamous Cell Carcinoma: A Bioinformatics Approach.Asian Pacific journal of cancer prevention : APJCP · 2026Article
- Molecular mechanisms of neutrophil regulatory network in anti-Candida infection.Frontiers in immunology · 2025Review
- Oral Cavity andPathogens (Basel, Switzerland) · 2022Review
- The microbial and host factors that govern Candida gastrointestinal colonization and dissemination.Current opinion in microbiology · 2021Review
- An IL-17F.S65L Knock-In Mouse Reveals Similarities and Differences in IL-17F Function in Oral Candidiasis: A New Tool to Understand IL-17F.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Oral epithelial IL-22/STAT3 signaling licenses IL-17-mediated immunity to oral mucosal candidiasis.Science immunology · 2020Article
- Post-sepsis immunosuppression depends on NKT cell regulation of mTOR/IFN-γ in NK cells.The Journal of clinical investigation · 2020Article
- Regulation of host-microbe interactions at oral mucosal barriers by type 17 immunity.Science immunology · 2020Review
- Advances in Understanding Human Genetic Variations That Influence Innate Immunity to Fungi.Frontiers in cellular and infection microbiology · 2020Review
- Nystatin enhances the immune response against Candida albicans and protects the ultrastructure of the vaginal epithelium in a rat model of vulvovaginal candidiasis.BMC microbiology · 2018Article
- Th17 cells differentiated with mycelial membranes of Candida albicans prevent oral candidiasis.FEMS yeast research · 2018Article
- EphA2 is an epithelial cell pattern recognition receptor for fungal β-glucans.Nature microbiology · 2018Article
- Pathogenesis of infections in HIV-infected individuals: insights from primary immunodeficiencies.Current opinion in immunology · 2017Review
- A Multifaceted Role of Tryptophan Metabolism and Indoleamine 2,3-Dioxygenase Activity inFrontiers in immunology · 2017Review
- The IDO-AhR Axis Controls Th17/Treg Immunity in a Pulmonary Model of Fungal Infection.Frontiers in immunology · 2017Article
- Sequential Dysfunction and Progressive Depletion of Candida albicans-Specific CD4 T Cell Response in HIV-1 Infection.PLoS pathogens · 2016Article
- Neutrophils Do Not Express IL-17A in the Context of Acute Oropharyngeal Candidiasis.Pathogens (Basel, Switzerland) · 2015Article
- Oropharyngeal Candidiasis in HIV Infection: Analysis of Impaired Mucosal Immune Response to Candida albicans in Mice Expressing the HIV-1 Transgene.Pathogens (Basel, Switzerland) · 2015Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe tissue-signaling cytokines IL-17 and IL-22 are critical to host defense against oral Candida albicans infection, by their induction of oral antimicrobial peptide expression and recruitment of neutrophils. Mucosal Th17 cells which produce these cytokines are preferentially depleted in HIV-infected patients. Here, we tested the hypothesis that defective IL-17- and IL-22-dependent host responses to C. albicans determine the phenotype of susceptibility to oropharyngeal candidiasis (OPC) in transgenic (Tg) mice expressing HIV-1.
resultsNaïve CD4+ T-cells and the differentiated Th1, Th2, Th17, Th1Th17 and Treg lineages were all profoundly depleted in cervical lymph nodes (CLNs) of these Tg mice. However, naive CD4+ cells from Tg mice maintained the capacity to differentiate into these lineages in response to polarizing cytokines in vitro. Expression of Il17, Il22, S100a8 and Ccl20 was enhanced in oral mucosal tissue of non-Tg, but not of Tg mice, after oral infection with C. albicans. Treatment of infected Tg mice with the combination of IL-17 and IL-22, but not IL-17 or Il-22 alone, significantly reduced oral burdens of C. albicans and abundance of Candida hyphae in the epithelium of tongues of infected Tg mice, and restored the ability of the Tg mice to up-regulate expression of S100a8 and Ccl20 in response to C. albicans infection.
conclusionsThese findings demonstrate that defective IL-17- and IL-22-dependent induction of innate mucosal immunity to C. albicans is central to the phenotype of susceptibility to OPC in these HIV transgenic mice.
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