[Immune response in dermatophytosis]

Abstract

A delayed-type hypersensitivity (DTH) response to a dermatophyte antigen is one of the host defense mechanisms. Peripheral blood mononuclear cells from patients with dermatophytosis produce a high level of IFN-gamma in response to stimulation with trichophytin. The presence of IFN-gamma mRNA in skin lesions of dermatophytosis was detected using reverse transcription-polymerase chain reaction. IFN-gamma-positive cells were observed immunohistochemically in the upper dermis of the skin lesions. These findings support the hypothesis that the skin lesions of dermatophytosis are associated with a Th1 response. The Th1 response, which is characterized by IFN-gamma release, is thought to be involved in the host defense against dermatophytes and to reflect cutaneous reaction in dermatophytosis. The stimulation of trichophytin significantly enhanced the release of IL-8 from keratinocytes. These findings account for the accumulation of neutrophils beneath the stratum corneum. The capacity of trichophytin-stimulated keratinocytes to release an enhanced level of IL-8 thus suggests that these cells can indeed help to induce the acute inflammatory response seen in dermatophyte infection. It therefore appears that keratinocytes not only play an important structural role in the formation of a physical barrier to dermatophytes but may also play an important functional role in initiating cutaneous inflammatory reactions, which might be involved in the host defense against dermatophytes. The production of IFN-gamma by peripheral blood mononuclear cells from patients with tinea unguium in response to stimulation with trichophytin was not impaired in contrast to that from patients without tinea unguium. Comparable lymphocyte proliferation with trichophytin was observed in both groups. No deficiency in Th1 response to dermatophyte antigen was shown in patients with tinea unguium by measuring the release of IFN-gamma, which plays a role in the effector phase of the DTH reaction. A deficiency of Th1 response to dermatophyte antigen, therefore, does not appear to play an important role in the establishment of tinea unguium.