Immunoregulation of T cell-mediated skin hypersensitivity

The recent extensive research on the different functions of T cells differing in cytokine production profiles has opened promising venues for further research on mechanisms and therapeutic options. Clearly, the routing hypothesis as described above still leaves many questions unanswered, such as the question why some chemicals may elicit strong Th2 responses and IgE antibody production even when applied to the skin, without apparent reduction of delayed allergic reactivity (Dearman et al., 1991). The preliminary understanding of regulatory mechanisms in allergic contact dermatitis has not yet led to further therapeutic progress. So far, no methods of permanent desensitization have been devised. Nevertheless, major cell types and mediators involved in allergic contact dermatitis have been identified. How T cells specifically recognize distinct allergens, and how these and other inflammatory cells interact to generate inflammation has begun to be understood. Moreover, the recently defined cellular interaction molecules and mediators provide promising targets for anti-inflammatory drugs. Obviously, drugs found to be effective in preventing severe T cell-mediated conditions, e.g. rejection of a vital organ graft, should be very safe before their use in allergic contact dermatitis would seem appropriate. To date, prudence favours any measure to prevent allergic contact dermatitis, be it through legal actions to outlaw the use of certain materials, or through avoiding personal contacts with these materials. In the meantime, for difficult-to-avoid allergens, further studies on the potential value of tolerogenic treatments should be intensified.