Dermatophytoses are superficial infections caused by a group of fungi, the dermatophytes, which invade keratinized tissue of skin, hair, and nails in humans and animals. The importance of normal immune function in resistance to dermatophytoses is substantiated by an increased susceptibility to chronic infection seen in patients with impaired immunological responses. Humoral and cell-mediated immunities are both elicited during the infection. However, specific antibodies to dermatophytes do not seem to play a major role in protective immunity. On the other hand, the development of cell-mediated immunity during the infection is critical in eliciting resistance to the disease. For instance, resolution of the disease in both naturally and experimentally infected humans and animals correlates with the development of delayed-type hypersensitivity (DTH), whereas persistence of infection is frequently accompanied by poor in vitro blastogenic response and absent DTH. Furthermore, in experimentally infected mice, immunity to dermatophyte infection can be achieved by adoptive transfer of lymphoid cells, but not by serum, of infected donors. The present review includes an overview of published work and current research on the cellular events implicated in immunity to dermatophytosis. The role of humoral factors in such immunoregulation is also discussed.

We have established a reproducible mouse model of dermatophytosis using Trichophyton quinckeanum. There was considerable variation in the pathogenic potential among 10 different strains of T. mentagrophytes or T. quinckeanum; susceptibility to the infection varied with the inbred strain of mouse used, with BALB/c or BALB/K mice proving to be the most susceptible. The primary infection was characterized by the development of a scutulum or crust consisting of large quantities of dermatophyte mycelium, dense infiltration with neutrophils, but minimal epidermal proliferation. By contrast, a secondary infection initiated 30 days after the primary infection showed different features with early and almost total elimination of fungal elements, a predominantly mononuclear cell response, and epidermal proliferation. If the secondary infection was given at the peak of the primary illness (day 7), there was a mononuclear cell response with epidermal proliferation but fungal mycelium was prominent and not quickly eliminated. The value of this model in investigating the kinetics of the immune response to experimental dermatophytosis is discussed.

A monoclonal antibody (Tq-1) that interacts with the phosphorylcholine (PC)-bearing antigens of Trichophyton quinckeanum was produced by fusion of myeloma cells (JKAg-8) with spleen cells of BALB/c mice immunized with an alum-precipitated fraction of T . quinckeanum cytoplasmic antigen. It was characterized as an IgM class antibody by immunodiffusion using anti-Ig heavy chain specific reagents, ELISA using immunoglobulin-specific peroxidaseconjugated antibodies, and by gel filtration chromatography; it showed high affinity for Staphylococcus aureus protein-A. Interaction of Tq-1 with PC-like antigens of T. quinckeanum was demonstrated by inhibition studies using ELISA, immunoblotting, immunoprecipitation and immuno electron microscopy techniques. The binding activity of Tq-1 antibody with a range of dermatophyte proteins was completely inhibited by prior incubation with PC hapten. Moreover, dermatophyte antigens reacting with the monoclonal antibody reacted strongly with sera from chronically infected mice. Dermatophyte antigens derived from both young (24 h) and old (20 d) cultures reacted with Tq-1 and this binding was inhibited by PC, suggesting that Tq-1 target antigen PC appears at an early stage during fungal growth and remains throughout its life.

Evidence is presented that T helper cells change their Lyt-1,2 phenotype, from Lyt-1+2- to Lyt-1-2+, during a secondary response. In a secondary adoptive transfer the Lyt phenotype of carrier-primed T cells was established before and after secondary challenge using monoclonal antibodies and both positive and negative selection in the fluorescence-activated cell sorter. In a carrier-primed donor, the T helper cells were Lyt-1+2- whereas 3 days after boosting the majority were Lyt-2+, and resistant to treatment with anti-Lyt-1 and complement. Parking experiments in lethally irradiated recipients confirmed that Lyt-2+ T helper cells were generated from Lyt-2- precursors. In a primary response, both Lyt-2- and Lyt-2+ T helper cells were present 4 to 20 days after immunization. Therefore T helper cells do not exhibit invariant expression of the Lyt-1,2 alloantigens.