Abstract
There is strong evidence that UV irradiation is a causal factor in human nonmelanoma skin cancer (1β3), and that immunosuppression is a high risk factor for skin cancer in humans (4,5). The use of animal model systems to investigate the sequence of events which lead to the induction and progression of skin tumors following chronic ultraviolet irradiation has clearly shown that the genotoxic effect of UV irradiation is only one of the components involved in this process. Immunological factors are also critically important in the pathogenesis of UV induced skin cancers (6,7). Most tumors induced by UV irradiation are highly antigenic and cannot grow in normal syngeneic mice. However, they can grow in immunodepressed or UV irradiated mice. The inability to reject antigenic, syngeneic UV-induced tumors can be transferred from UV irradiated mice to naive recipients with splenocytes bearing an Lyt-1+, Lyt-2β, L3T4+, Iaβ, henotype(8). This anergy has been found to be critical in photocarcinogenesis (9). Significantly, the suppression induced by UV irradiation appears to be restricted to contact hypersensitivity reactions and rejection of tumors induced by UV radiation or some chemicals (10,11). Antibody formation, mitogen reactivity, and allograft rejection are reported to be normal in UV irradiated mice (12β14).
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Gensler, H.L. (1990). Reduction of Ultraviolet-Induced Immunosuppression and Enhanced Resistance to Ultraviolet-Induced Tumors by Retinyl Palmitate and Canthaxanthin. In: Prasad, K.N., Meyskens, F.L. (eds) Nutrients and Cancer Prevention. Experimental Biology and Medicine, vol 23. Humana Press. https://doi.org/10.1007/978-1-4612-4516-2_12
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