Ultraviolet radiation and tumor immunity.

摘要

Ultraviolet (UV) radiation induces a specific tolerance toward UV-induced skin tumors. This phenomenon has been known and studied for more than 25 years, but the mechanisms by which protective tumor immunity or tumor tolerance is induced are still largely obscure. In parallel with these studies, short-term assays on UV-induced immunosuppression and tolerance toward simple chemicals (e.g., dinitrochlorobenzene) have been analyzed, particularly with respect to the role of cytokines (most notably, interleukin (IL)-10 vs IL-12). However, these short-term assays are not likely to be fully adequate models of the long-term UV-induced tumor tolerance. The important nodal points of action in these immune reactions appear to be the T cells and the antigen-presenting cells (APCs) that prime them. The main focus should probably be on CD8(+) T cells as the ultimate effector of the cytotoxic response against UV-induced skin cancers. APC-mediated activation of these cells depends strongly on cosignaling of CD4(+) T cells. In a tumor tolerant state the activity of the cytotoxic CD8(+) T cells appears to be inhibited through CTLA-4(+) and natural killer T cells. The latter cells are CD1-restricted, which indicates the importance of "unconventional" antigens to UV-induced tumor tolerance.