Callahan G N, Leach D R
Department of Pathology, Colorado State University, Fort Collins 80524, USA.
Cancer Detect Prev. 1996;20(3):199-206.
Tumor cells typically fail to stimulate protective immune response in the autochthonous host. This does not appear to be the result of either inadequate antigenicity or failure to express a normal complement of major histocompatibility complex (MHC) class 1 molecules. To investigate if tumor cells fail to stimulate protective immunity because they fail to activate adequate numbers of T helper cells, we transfected murine fibrosarcoma and melanoma cells with genes encoding syngeneic and allogeneic MHC class II molecules. Fibrosarcoma cells expressing either type of MHC class II molecules failed to induce tumors in syngeneic mice and stimulated T helper cell-dependent antitumor immune responses that protected mice from subsequent challenge with untransfected tumor cells. The antitumor response involved both CD4+ and CD8+ T cells, and appeared to be dependent on at least low levels of innate tumor cell immunogenicity.
肿瘤细胞通常无法在宿主体内刺激产生保护性免疫反应。这似乎既不是抗原性不足的结果，也不是未能表达正常数量的主要组织相容性复合体（MHC）I类分子的结果。为了研究肿瘤细胞是否因未能激活足够数量的辅助性T细胞而无法刺激保护性免疫，我们用编码同基因和异基因MHC II类分子的基因转染了小鼠纤维肉瘤和黑色素瘤细胞。表达任何一种MHC II类分子的纤维肉瘤细胞均无法在同基因小鼠中诱导肿瘤，并刺激了辅助性T细胞依赖性抗肿瘤免疫反应，从而保护小鼠免受未转染肿瘤细胞的后续攻击。抗肿瘤反应涉及CD4+和CD8+ T细胞，并且似乎至少依赖于低水平的先天性肿瘤细胞免疫原性。
