Slater L M, Sweet P, Stupecky M, Reynolds J T
Department of Medicine, University of California at Irvine 92717, USA.
Clin Immunol Immunopathol. 1995 Jun;75(3):239-45. doi: 10.1006/clin.1995.1077.
The role of the immune response in the chemotherapeutic cure of an intact host with neoplasia is not well defined. We have previously shown that the addition of cyclosporin A to VP-16 therapy of BDF/1 mice with L1210 leukemia produces immunity to leukemia in long-surviving host animals. We now characterize this immunity as being tumor specific and related to the participation of CD8 T-lymphocytes. Splenocytes derived from L1210 leukemia immune mice are cytotoxic to L1210 cells after in vitro restimulation, compared to splenocytes harvested from nonimmune control mice. This cytotoxicity is lost by CD8 T-lymphocyte depletion and persists in Ia antigen blocking experiments. Cytotoxicity is selective for L1210 leukemia compared to P388 leukemia, an alternate Ia antigen expressing methylcholanthrine-induced acute lymphoid leukemia, and L1210 leukemia-immune mice remain susceptible to P388 leukemia in vivo demonstrating specificity of the immune response generated by cyclosporin A/VP-16 therapy.
免疫反应在完整宿主的肿瘤化疗治愈过程中的作用尚未明确界定。我们之前已经表明，在BDF/1小鼠的L1210白血病VP - 16治疗中添加环孢素A会使长期存活的宿主动物产生对白血病的免疫力。我们现在将这种免疫力表征为肿瘤特异性的，并且与CD8 T淋巴细胞的参与有关。与从非免疫对照小鼠收获的脾细胞相比，来自L1210白血病免疫小鼠的脾细胞在体外再刺激后对L1210细胞具有细胞毒性。这种细胞毒性在CD8 T淋巴细胞耗竭后丧失，并在Ia抗原阻断实验中持续存在。与P388白血病相比，细胞毒性对L1210白血病具有选择性，P388白血病是另一种表达Ia抗原的甲基胆蒽诱导的急性淋巴细胞白血病，并且L1210白血病免疫小鼠在体内对P388白血病仍然易感，这证明了环孢素A/VP - 16治疗产生的免疫反应的特异性。
