ULTRAVIOLET RADIATION INDUCED SKIN CANCER

紫外线诱导的免疫抑制和遗传损伤都是已知的 会导致人类和实验动物的皮肤癌。故障： 紫外线照射癌前病变后皮肤免疫系统的反应 携带新抗原的细胞可能在发育过程中起重要作用。 皮肤癌。紫外线照射对迟发型超敏反应的抑制作用 (DTH)在功能上相似，可以作为一种标志来确定 个体对紫外线诱导的免疫抑制的易感性是一种风险 诱发人类和部分小鼠皮肤癌的因素 菌株。此外，UVR还可诱导DNA损伤和个体DNA修复 效率也可能导致宿主对皮肤癌的易感性。 最近的证据表明 肿瘤坏死因子α(TNFpha)可能介导UVR诱导 在人和选定品系的小鼠中迟发型超敏反应的免疫抑制。 肿瘤坏死因子α基因座(内含子1、BamHI RFLP和a 5.

Both UVR induced immunosuppression and genetic damage are known to contribute to skin cancer in humans and experimental animals. Failure of the skin immune system to respond after UVR exposure to preneoplastic cells bearing neoantigens may contribute significantly to the development of skin cancer. UVR induced suppression of delayed-type hypersensitivity (DTH) is functionally similar and may be used as a marker to determine individual susceptibility to UV-induced immunosuppression as a risk factor for the induction of skin cancer in humans and selected mouse strains. In addition, UVR induced DNA damage and individual DNA repair efficiencies may also contribute to host susceptibility for skin cancer. Recent evidence indicates that tumor necrosis factor alpha (TNFalpha) may mediate UVR induced immune suppression of DTH in humans and in selected strains of mice. Genetic polymorphisms at the TNFalpha locus (intron 1 BamHI RFLP and a 5