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.