Fungal skin infections significantly contribute to the global human disease burden, yet our understanding of cutaneous immunity against dermatophytes remains limited. Previously, we developed a model of epicutaneous infection with Microsporum canis in C57BL/6 mice, which highlighted the critical role of IL-17RA signaling in anti-dermatophyte defenses. Here, we expanded our investigation to the human pathogen Nannizzia gypsea and demonstrated that skin γδTCRint and CD8/CD4 double-negative βTCR+ T cells are the principal producers of IL-17A during dermatophytosis.
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