Daynes R A, Spellman C W, Woodward J G, Stewart D A
Transplantation. 1977 Apr;23(4):343-8. doi: 10.1097/00007890-197704000-00008.
The majority of skin tumors induced in mice by ultraviolet (UV) light are rejected when implanted into normal syngeneic recipients. Subcarcinogenic levels of UV light exposure render the normally resistant mice susceptible to tumor challenge. The immunoregulatory effect of UV light appears to be additive, since the growth rate of a tumor transplant is dependent upon the length of UV exposure administered prior to implantation. This suppressive influence does not appear to be directly mediated by the UV light, because the amputation of UV-irradiated tail skin allows for a retention of tumor resistance in otherwise tumor-susceptible hosts. UV-irradiated mice could also be immunized against UV tumors, which suggests that immune recognition of tumor-specific transplantation antigens has not been inhibited. The ability of UV exposure to alter normal immunological reactivity to UV-induced tumors is possibly an integral factor in the mechanism underlying UV carcinogenesis.
紫外线(UV)诱导小鼠产生的大多数皮肤肿瘤,植入同基因正常受体后会被排斥。亚致癌水平的紫外线照射会使原本具有抵抗力的小鼠易受肿瘤攻击。紫外线的免疫调节作用似乎具有累加性,因为肿瘤移植的生长速度取决于植入前给予的紫外线照射时长。这种抑制作用似乎并非直接由紫外线介导,因为切除经紫外线照射的尾部皮肤后,原本易患肿瘤的宿主仍能保持肿瘤抵抗力。经紫外线照射的小鼠也能针对紫外线诱导的肿瘤进行免疫,这表明对肿瘤特异性移植抗原的免疫识别并未受到抑制。紫外线暴露改变对紫外线诱导肿瘤的正常免疫反应的能力,可能是紫外线致癌机制的一个重要因素。