A MONOCLONAL-ANTIBODY TO CIS-UROCANIC ACID PREVENTS THE ULTRAVIOLET-INDUCED CHANGES IN LANGERHANS CELLS AND DELAYED-HYPERSENSITIVITY RESPONSES IN MICE, ALTHOUGH NOT PREVENTING DENDRITIC CELL ACCUMULATION IN LYMPH-NODES DRAINING THE SITE OF IRRADIATION AND CONTACT HYPERSENSITIVITY RESPONSES

Ultraviolet B (UVB) irradiation of C3H mice causes suppression of dela yed hypersensitivity and contact hypersensitivity (CH) to antigens enc ountered following exposure, and is accompanied by a reduction in Lang erhans cell (LC) numbers in the epidermis, loss of epidermal antigen-p resenting cell function, and accumulation of dendritic cells in lymph nodes draining the site of irradiation. Various photoreceptors and med iators of these changes have been proposed, one of which is cis-urocan ic acid (cis-UCA) formed from the naturally occurring trans-UCA in the epidermis on UV irradiation. A monoclonal antibody that reacts with c is-UCA has become available recently and has been used in this study t o clarify the role of UCA. Pretreatment of C3H mice with the monoclona l antibody abrogated the UVB-induced and cis-UCA-induced reduction in epidermal LC numbers. It also prevented the UV-induced suppression of epidermal antigen-presenting cell ability as measured by the mixed ski n lymphocyte response. However, it had no effect on the accumulation o f dendritic cells in lymph nodes draining the site of UV exposure. Wit h regard to hypersensitivity responses, it did not prevent UV-induced suppression of CH to oxazolone at a range of concentrations but it res tored to normal the UV-suppressed delayed hypersensitivity to herpes s implex virus, if administered before exposure. Thus cis-UCA is involve d in some UV-induced changes in murine skin but not in others, where a lternative mediators, such as tumor necrosis factor-alpha, may be more important.