CD4+ anti-tumor T cells reactive with rat adenocarcinoma 13762 kill tumor in vitro and cause regression of tumor in vivo. The role of various host immune cells in CD4+ T-cell-mediated tumor elimination in vivo was investigated by adoptive transfer of anti-tumor T cell clones to recipients that were selectively depleted of individual immune cell types. By these means, macrophages and NK cells were found to be required for tumor killing. Depletion of host CD4+ T cells, CD8+ T cells, or neutrophils was without effect on tumor elimination by anti-tumor T cells. An essential role for antigen receptor-negative NK cells is likely dependent upon secretion of IFN-gamma from NK cells since treatment of tumor recipients with anti-IFN-gamma antibody prior to adoptive transfer and tumor challenge abrogated T cell killing, resulting in progressive tumor growth. Viability of adenocarcinoma 13762 or anti-tumor T cells was unaffected by treatment with either IFN-gamma or anti-IFN-gamma antibody in vitro, but cell surface MHC class II expression was induced in tumor cells by exposure to IFN-gamma. In addition, tumor cells were isolated from tumor-bearing animals by absorption using anti-MHC class II antibody, demonstrating that 13762 tumor expresses cell surface MHC class II antigens in situ. However, if hosts were depleted of NK cells before tumor challenge, MHC class II+ tumor was not recovered. Collectively these results suggest that adenocarcinoma 13762 is eliminated by MHC class II-restricted CD4+ T cells by direct tumor killing.

译文

与大鼠腺癌13762反应的CD4抗肿瘤T细胞在体外杀死肿瘤并在体内引起肿瘤消退。通过将抗肿瘤T细胞克隆过继转移到选择性清除了个体免疫细胞类型的受体上,研究了各种宿主免疫细胞在体内CD4 T细胞介导的肿瘤消除中的作用。通过这些手段,发现杀死肿瘤需要巨噬细胞和NK细胞。宿主CD4 T细胞,CD8 T细胞或嗜中性白细胞的耗竭对抗肿瘤T细胞对肿瘤的消除没有影响。抗原受体阴性NK细胞的重要作用可能取决于NK细胞分泌IFN-γ,因为在过继转移和肿瘤攻击之前用抗IFN-γ抗体治疗肿瘤受体可以消除T细胞杀伤,从而导致进行性肿瘤生长。体外用IFN-γ或抗IFN-γ抗体治疗不会影响腺癌13762或抗肿瘤T细胞的存活率,但通过暴露于IFN-γ诱导了肿瘤细胞的细胞表面MHC II类表达。另外,通过使用抗MHC II类抗体的吸收从荷瘤动物中分离出肿瘤细胞,表明13762肿瘤原位表达细胞表面MHC II类抗原。但是,如果宿主在肿瘤攻击前已耗尽NK细胞,则无法恢复MHC II类肿瘤。这些结果共同表明,通过直接杀死肿瘤,MHC II类限制性CD4 T细胞可消除13762腺癌。

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