Murahata R I, Mitchell M S
J Natl Cancer Inst. 1982 Sep;69(3):607-12.
The ability of iv administered BCG to antagonize immunosuppression caused by injection of the antimetabolite cytarabine (beta-cytosine arabinoside; ara-C) was investigated in C57BL/6 mice. Treatment with BCG 10 days before alloimmunization with killed L1210 tumor cells decreased spleen T-cell-mediated cytolysis against allogeneic P815Y tumor cells, as measured by a short-term 51Cr release assay, and potentiated immunosuppression due to ara-C. In contrast, spleen cell-mediated immunity (CMI) that was assayed by a 48-hour microcytotoxicity assay (MCA) was augmented by systemic BCG administered before alloimmunization. Pretreatment with BCG resulted in a complete and long-lasting protection against the immunosuppressive effects of ara-C on this CMI as measured by the MCA. Treatment with BCG after cytoreductive therapy resulted in a significant, although transient, reversal of immunosuppression. Depending on the type of response and thus the type of effector cell measured, BCG acts as a moderate immunosuppressive agent or a strong immunopotentiator of CMI.
在C57BL/6小鼠中研究了静脉注射卡介苗（BCG）拮抗注射抗代谢物阿糖胞苷（β-胞嘧啶阿拉伯糖苷；ara-C）所引起的免疫抑制的能力。在用灭活的L1210肿瘤细胞进行同种免疫前10天用BCG治疗，通过短期51Cr释放试验测定，可降低脾脏T细胞介导的对同种异体P815Y肿瘤细胞的细胞溶解作用，并增强了ara-C所致的免疫抑制。相反，通过48小时微细胞毒性试验（MCA）测定的脾脏细胞介导免疫（CMI）在同种免疫前通过全身给予BCG而增强。如通过MCA所测定，用BCG预处理可对ara-C对该CMI的免疫抑制作用产生完全且持久的保护。在减瘤治疗后用BCG治疗导致免疫抑制有显著的（尽管是短暂的）逆转。根据反应类型以及所测定的效应细胞类型，BCG可作为CMI的中度免疫抑制剂或强效免疫增强剂。
