Thorn R M
J Immunol. 1978 Nov;121(5):1920-6.
Cytotoxic responses of UV-irradiated mice against syngeneic UV-induced tumors were measured by using a 51Cr-release assay to determine if UV treatment induced a specific reduction of cytotoxic activity. The in vivo and in vitro primary responses against syngeneic tumors and allogeneic cells were unaffected, as was the "memory" response (in vivo stimulation, in vitro restimulation) against alloantigens. In contrast, the memory response of UV-treated mice against syngeneic, UV-induced tumors was consistently and significantly depressed. The cytotoxicity generated by tumor cell stimulation in vivo or in vitro was tumor-specific and T cell-dependent. Since the primary response against syngeneic UV-induced tumors produces apparently normal amounts of tumor-specific cytotoxic activity, UV-treated mice may not reject transplanted syngeneic tumors because of too few T effector memory cells. These results imply that, at least in this system, tumor rejection depends mostly on the secondary responses against tumor antigens and that at least one carcinogen can, indirectly, specifically regulate immune responses.
通过使用51Cr释放试验来测定紫外线照射小鼠对同基因紫外线诱导肿瘤的细胞毒性反应,以确定紫外线处理是否导致细胞毒性活性的特异性降低。对同基因肿瘤和异基因细胞的体内和体外初级反应未受影响,对同种异体抗原的“记忆”反应(体内刺激,体外再刺激)也是如此。相比之下,紫外线处理小鼠对同基因紫外线诱导肿瘤的记忆反应持续且显著降低。体内或体外肿瘤细胞刺激产生的细胞毒性具有肿瘤特异性且依赖于T细胞。由于对同基因紫外线诱导肿瘤的初级反应产生的肿瘤特异性细胞毒性活性明显正常,紫外线处理的小鼠可能由于T效应记忆细胞过少而无法排斥移植的同基因肿瘤。这些结果表明,至少在这个系统中,肿瘤排斥主要取决于对肿瘤抗原的二次反应,并且至少一种致癌物可以间接特异性调节免疫反应。