Romani L, Grohmann U, Puccetti P, Rossi M A, Fioretti M C
Department of Experimental Medicine and Biochemical Sciences, University of Perugia, Italy.
Int J Immunopharmacol. 1990;12(7):743-9. doi: 10.1016/0192-0561(90)90037-n.
Xenogenized variant cells (L5178Y/DTIC) of a murine lymphoma line confer a high degree of specific protection against subsequent challenge of mice with parental L5178Y cells. In an attempt to better define the effect of DTIC-induced determinants on parental antigen recognition and the mechanisms involved in this protection, we evaluated the frequency of anti-parental tumor cytotoxic T lymphocyte precursors following priming of mice with xenogenized cells in vivo. In addition, we tested the effect of host sensitization with the immunogenic, retrovirus-related proteins that are precipitated from the surface of L5178Y/DTIC cells by means of specific antibody. Our results indicated that the novel determinants induced by DTIC treatment on L5178Y cells do not act as helper determinants for the generation of tumor-specific cytotoxic responses. Therefore, increased frequency of tumor-specific cytotoxic lymphocytes does not seem to be a major mechanism of anti-parental tumor immunity induced by xenogenized variant cells.
小鼠淋巴瘤细胞系的异种化变异细胞(L5178Y/DTIC)对随后用亲代L5178Y细胞攻击的小鼠具有高度特异性保护作用。为了更好地确定达卡巴嗪诱导的决定簇对亲代抗原识别的影响以及这种保护作用的相关机制,我们评估了在体内用异种化细胞免疫小鼠后抗亲代肿瘤细胞毒性T淋巴细胞前体的频率。此外,我们测试了用特异性抗体从L5178Y/DTIC细胞表面沉淀出的免疫原性逆转录病毒相关蛋白对宿主致敏的影响。我们的结果表明,达卡巴嗪处理在L5178Y细胞上诱导的新决定簇不作为产生肿瘤特异性细胞毒性反应的辅助决定簇。因此,肿瘤特异性细胞毒性淋巴细胞频率的增加似乎不是异种化变异细胞诱导的抗亲代肿瘤免疫的主要机制。