We believe that epidermal LC in normal skin can present antigen more effectively to T cells that mediate "cellular" immunity (e.g., Th1 cells) than to T cells that promote "humoral" immunity (e.g., Th2 cells). Circumstantial evidence supporting this hypothesis include the observations that most immune responses that are initiated in skin are T cell rather than B cell mediated, and that most, if not all, reported immunosuppressive effects of UVB radiation affect T cell rather than B cell responses. A second hypothesis is that the suppressive effects of UVB radiation on cutaneous immune responses are due to altered antigen presentation by LC. Our work with CD4+ Th1 and Th2 clones suggests that the long-lasting tolerance induced by UVB radiation in contact allergy and DTH assays may be explained by the induction by UVB-irradiated LC of clonal anergy in Th1 cells. It is also possible that Th2 cells, whose proliferative capacity remain intact despite exposure to UVB-irradiated LC, exert additional suppressive effects on Th1 cells. Finally, we consider the tolerogenic APC function of UVB-irradiated LC to serve two consequences. A detrimental effect occurs when it precludes proliferation of T cells that specifically recognize tumor antigens or infectious agents. On the other hand, a beneficial result might be produced when it prevents clonal expansion of T cells reactive to autoantigens, especially those that may emerge in epidermis following exposure to UVB radiation.
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