| Summary: | Exposure to ultraviolet-B light (UVB) suppresses immune responses to a variety of antigens, including contact sensitizers, in both mice and humans. A number of mediators of UVB-induced immunosuppression have been proposed including DNA damage, <I>cis</I>-urocanic acid, TNF-α and IL-10. UVB irradiation also causes the loss of Langerhans cells (LC) from the skin and the accumulation of LC-derived dendritic cells (CD) in the draining lymph nodes (DLN). A chronic UVB exposure protocol, using broadband (270-350nm) and narrowband (311-312nm) sources, was used to examine the effect of UVB on the skin immune system. Exposure to both sources reduced the numbers of LC in the epidermis. Exposure to broadband but not narrowband UVB induced epidermal thickening in a dose dependent manner. Although damage measured by thickening resulted from broadband UVB only, both sources led to a small increase in sunburn cells, which may represent an apoptotic keratinocyte population. Both sources were equally efficient at inducing the conversation of <I>trans</I>-urocanic acid to the <I>cis</I>-isomer, but only the broad band source suppressed contact hypersensitivity (CH) responses. Thus LC loss and the isomerization of urocanic acid may not be the primary mediators of immunosuppression during chronic UVB exposure. An acute UVB exposure protocol was used to examine the effect of UVB on DC <I>in vivo. </I> Mice were irradiated with an immunosuppressive dose of UVB, and the function and phenotype of DC accumulating in the DLN was examined. Exposure to UVB prior to sensitization did not reduce the ability of DC to induce proliferative responses of hapten sensitized lymph node cells (LNC). The necessary function of DC in mixed lymphocyte reactions was also unaffected by prior exposure to an immunosuppressive dose of UVB. The expression of MHC class II, intercellular adhesion molecule-1 and B7-2 (CD86) on DC was also examined.
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