Immunological resistance to dermatophyte infections

Abstract

Dermatophytic fungus infections are common and in the main confined to the stratum corneum. The way the body keeps these infections confined to the stratum corneum involves both nonspecific and specific factors. Cell-mediated immune reactions appear to be the major host defense against invasion. Appropriate cell-mediated immunity not only can limit the spread of dermatophytic fungi but also can rid the fungus from host skin. In contrast, the absence of cell-mediated immunity predisposes to severe and widespread infection and to chronic infection. Complement and polymorphonuclear leukocytes can interact with hyphae once they invade into viable tissue. These interactions are inhibitory to growth. In addition, the inflammation provoked by these interactions can increase epidermal turnover time and thereby force retreat of the fungus back into the stratum corneum or rid the fungus through desquamation. The role of specific antibodies to dermatophytic fungi is uncertain, but it is likely a minor one. High levels of antibodies do not protect against infection or allow resolution of established infection in the absence of other mechanisms. Antibodies may augment complement activation and accumulation of polymorphonuclear leukocytes, but it is unlikely they contribute directly to killing. Indeed, IgE antibodies to dermatophytic fungi develop in many patients with chronic infections.