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<p><i>Candida albicans</i> is a common resident of the microbiota that supports host homeostasis but can cause disease when immune defences are impaired. Mucocutaneous candidiasis in individuals with IL-17 immune defects provides insights into the immune system’s role in controlling <i>C. albicans</i>. Here, using a murine model of oral colonization, we show that IL-17 signalling maintains <i>C. albicans</i> in a non-pathogenic state. Loss of IL-17 leads to fungal filamentation and upregulation of hyphae-associated genes, which is accompanied by epithelial barrier disruption and inflammation, linked to aberrant IL-22 and IL-13 production. The emergence of pathogenic fungal traits was associated with impaired zinc chelation due to reduced calprotectin expression in the IL-17-deficient mice. Prolonged exposure to the immune-dysregulated tissue led to selection of stable, damage-inducing <i>C. albicans</i> variants, mirroring the evolution of isolates from a chronic mucocutaneous candidiasis patient. These findings reveal how IL-17 protects against fungal pathogenicity and how immune dysfunction fosters <i>C. albicans</i> adaptation and diversification within the host.</p>

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IL-17-mediated antifungal immunity restricts Candida albicans pathogenicity in the oral cavity

  • 期刊论文

  • 发表日期：

    2025年12月12日

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  • Ricardo Fróis-Martins,
  • Kontxi Martinez de San Vicente,
  • Corinne Maufrais,
  • Sarah Mertens,
  • Natacha Sertour,
  • Emilie Sitterlé,
  • Marie-Elisabeth Bougnoux,
  • Christophe d’Enfert,
  • Salomé LeibundGut-Landmann

摘要

Candida albicans is a common resident of the microbiota that supports host homeostasis but can cause disease when immune defences are impaired. Mucocutaneous candidiasis in individuals with IL-17 immune defects provides insights into the immune system’s role in controlling C. albicans. Here, using a murine model of oral colonization, we show that IL-17 signalling maintains C. albicans in a non-pathogenic state. Loss of IL-17 leads to fungal filamentation and upregulation of hyphae-associated genes, which is accompanied by epithelial barrier disruption and inflammation, linked to aberrant IL-22 and IL-13 production. The emergence of pathogenic fungal traits was associated with impaired zinc chelation due to reduced calprotectin expression in the IL-17-deficient mice. Prolonged exposure to the immune-dysregulated tissue led to selection of stable, damage-inducing C. albicans variants, mirroring the evolution of isolates from a chronic mucocutaneous candidiasis patient. These findings reveal how IL-17 protects against fungal pathogenicity and how immune dysfunction fosters C. albicans adaptation and diversification within the host.