Cell-mediated immunity in the immunopathogenesis of dermatophytosis

CMI to dermatophyte antigens, principally trichophytin, is central to both (1) pathogenesis of the typical "ringworm" lesion and (2) an acquired, relative resistance that affords partial immunity to the host. The exact form of effector "T" cell immunity and the cellular and molecular mechanism(s) which eliminate dermatophytes from the skin, are poorly understood, but may involve lymphokine and accelerated epidermal turnover. Recent studies in the "nude" rat suggest that this thymic deficient animal offers potential for study of chronic, extensive dermatophytosis. The pathogenesis of the indolent inflammation of chronic infection is unclear, but may involve fungal derived chemotactic factors and/or activation of the alternative complement pathway. Chronic, extensive dermatophytosis may be caused by several different organisms, including T. rubrum, T. mentagrophytes, T. tonsurans and T. concentricum. Despite the multiple, microbial etiologies, most patients with this distinctive syndrome share similar immunological characteristics, including deficient, antigen-specific CMI to trichophytin. Approximately half of the patients have either an immediate hypersensitivity to trichophytin or an elevated serum IgE level, and in addition, they exhibit other stigmata of atopy including a positive family history. It is intriguing to consider the possibility that genetic control of the immune response may render a certain IgE hyperresponsive subpopulation unable to mount sufficient host resistance to reject dermatophyte infection.