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The precise mechanism of the host defense that protects the nail from dermatophyte invasion is not known. Recent immunological findings in dermatophytosis suggest the hypothesis that the T helper 1 (Th1) response may play a role in protecting the nail from dermatophyte invasion. Our present study focused on interferon-gamma (IFN-gamma) release in patients with tinea pedis with or without tinea unguium, and pathogenesis of tinea unguium is discussed in relation to the association with a possible deficiency of Th1 response in the host defense mechanism. The production of IFN-gamma by peripheral blood mononuclear cells from the patients with tinea unguium in response to stimulation with trichophytin was not impaired in contrast to that from the patients without tinea unguium. Comparable lymphocyte proliferation to trichophytin was observed in both groups. Normal healthy persons with no clinical evidence of tinea could be divided into two groups based on lymphocyte proliferation and IFN-gamma production in response to trichophytin: high responder and low responder, with high responders being correlated with a clinical history of previous tinea pedis. In this study, a lack of a Th1 response to dermatophyte antigen was not shown in patients with tinea unguium by measuring the release of IFN-gamma, which plays a role in the effector phase of the delayed-type hypersensitivity reaction. A deficiency in the Th1 response to dermatophyte antigen, therefore, does not appear to play an important role in the establishment of tinea unguium.

Interferon-? production in peripheral lymphocytes of patients with tinea pedis: comparison of patients with and without tinea unguium