Dermatophytosis, or tinea, is a common superficial fungal infection affecting people of all ages worldwide. It is caused by keratinophilic dermatophytes that invade the skin barrier, colonize keratinized tissues, and activate host immune responses, leading to inflammation and tissue damage. Understanding the molecular pathogenesis is critical for standardizing treatment and developing targeted therapies. Key aspects include fungal invasion mechanisms, adhesion and proliferation on skin, secreted molecules, virulence factors, colonization patterns, and host-pathogen interactions. As new dermatophyte species emerge, advanced techniques are needed to study gene expression regulation during infection, disease progression, and how fungal factors modulate the host immune response, particularly in keratinocytes. Functional annotation of dermatophyte genes and their human counterparts is essential to map these interactions. This review summarizes the most common clinical forms of dermatophytosis, discusses selected host-dermatophyte interactions and evolutionary adaptations, and highlights current strategies for diagnosis and therapy. A deeper comprehension of these mechanisms will help in designing precise antifungal drugs and improving disease management.
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Sarkar et al. (2026) studied this question.
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