Conclusion

Most of the published studies indicate the inhibitory effects of UV irradiation, especially on cellular immune responses. However, UV exposure is also known to induce and activate cell-mediated diseases such as systemic and certain forms of cutaneous LE. Thus, it seems that there is a paradox in the effects of UV irradiation on health. However, systemic LE, for example, is thought to represent a Th2-type disease with increased autoantibody production and B-cell activation, resulting in cutaneous inflammation, as well as internal organ involvement. For efficient B-cell activation and (auto-)antibody production, help from T cells, especially Th2 cells, is required. Because UV irradiation induces a shift toward Th2 rather than Th1 immune responses and Th2 cells have been shown to be involved in the activation of B cells, it might be possible that UV-induced/activated Th2 cells contribute to the development and/or deterioration of LE after UV light exposure. Furthermore, IL-10 represents an important growth factor for B cells. Multiple investigations have demonstrated up-regulation of IL-10 production after UV irradiation in mice and humans. Therefore, it would be possible that UV-induced IL-10 production contributes to B-cell survival under certain circumstances and thereby contributes to disease development. Together, these findings suggest how UV light exposure might be able to induce and/or exacerbate autoimmune disorders.

Acknowledgements. Due to space limitations, many studies could not be referenced or mentioned. We apologize to their authors. This work was supported by the German Research Association (DFG) project BE 1580/2-3, SFB 293, IZKF grant Lo2/065/04, and a European Community Grant QLK4-CT-2001-00115.

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