Current knowledge of host response in human tinea

Skin infection caused by dermatophytes is called tinea. In this short review, the known mechanisms and factors involved in human tinea and important for the host response are briefly delineated. To establish tinea, fungal propagules must attach to the skin, germinate and overcome the epidermal barrier. Keratinases and other enzymes are released in this process and host keratinocytes are activated. This is followed by an inflammatory response mediated by a plentitude of cytokines and receptors, comprising innate as well as acquired immunity, including neutrophilic granulocytes, macrophages, antibodies and T cells. Cellular defence mechanisms appear to be decisive for clearing of infection. Nails and hair follicles are the particular sites often invaded by dermatophytes that show distinctive patterns of infection. Nails are largely excluded from defence mechanisms and steroid hormones of the pilosebaceous units may have a particular effect on follicular infection. Fungal invasion of the dermis can cause granulomatous reactions. Immune reactions to dermatophytes may lead to sterile eruptions distant from the infected skin areas.