Daynes R A, Bernhard E J, Gurish M F, Lynch D H
J Invest Dermatol. 1981 Jul;77(1):77-85. doi: 10.1111/1523-1747.ep12479260.
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 light (UVL) exposure has clearly shown that the direct mutagenic effects of UVL is only one of the components involved in this process. In spite of the fact that overt carcinogenesis is only one of the many effects produced by UV light, most hypotheses as to the mechanism by which UVL can cause the mutations necessary to achieve the transformed phenotype have focused on the direct effects of UVL on DNA and the generation of carcinogenic compounds. Investigations during the last 5 yr, however, have clearly demonstrated that immunologic factors are also critically important in the pathogenesis of UV-induced skin cancers. A complete understanding of UV-carcinogenesis must therefore consider the mechanisms which allow the transformed cell to evade immunologic rejection by the host in addition to those aspects which deal with conversion of a normal cell to a cancer cell. It is the object of this review to provide both a historical account of the work which established the immunologic consequences of chronic UVL exposure and the results of recent experiments designed to investigate the kinetics and mechanisms by which UVL affects the immunologic apparatus. In addition, a hypothetical model is presented to explain the sequence of events which ultimately lead to the emergence of the suppressor T-cells which regulate antitumor immune responses.
利用动物模型系统来研究长期紫外线（UVL）照射后导致皮肤肿瘤诱发和进展的一系列事件，结果清楚地表明，UVL的直接诱变作用只是这一过程中涉及的因素之一。尽管明显的致癌作用只是紫外线产生的众多效应之一，但关于UVL导致实现转化表型所需突变的机制的大多数假说都集中在UVL对DNA的直接作用以及致癌化合物的生成上。然而，过去5年的研究清楚地表明，免疫因素在紫外线诱导的皮肤癌发病机制中也至关重要。因此，要全面理解紫外线致癌作用，除了考虑涉及正常细胞转化为癌细胞的那些方面外，还必须考虑使转化细胞逃避宿主免疫排斥的机制。本综述的目的是既提供关于确定长期UVL照射免疫后果的研究工作的历史记述，也提供旨在研究UVL影响免疫机制的动力学和机制的近期实验结果。此外，还提出了一个假说模型，以解释最终导致调节抗肿瘤免疫反应的抑制性T细胞出现的一系列事件。
