Fishelson Z, Berke G
J Immunol. 1981 May;126(5):2048-52.
Tumor overgrowth in spite of an ongoing antitumor immune response may be due to a basic immunologic defect in T cell-mediated responses against the potentially immunogenic tumor cells. To further understand T cell-mediated responses in syngeneic tumor-host systems, we have analyzed the interaction of cytotoxic T lymphocytes (CTL) with syngeneic tumor cells and have compared it with CTL-allogeneic tumor cell interaction. The major conclusions of this study are: 1) Syngeneic and allogeneic CTL lyse target cells through a similar mechanism. 2) The reduced reactivity in the syngeneic system is due to the low content of effector cells capable of binding to and killing tumor cells. 3) The avidity of CTL-syngeneic tumor cell binding is lower than CTL-allogeneic tumor cell binding. We suggest that the latter 2 observations result from a low immunogenicity of tumor cells in the syngeneic host.
尽管存在持续的抗肿瘤免疫反应,但肿瘤仍过度生长,这可能是由于针对潜在免疫原性肿瘤细胞的T细胞介导反应存在基本的免疫缺陷。为了进一步了解同基因肿瘤-宿主系统中T细胞介导的反应,我们分析了细胞毒性T淋巴细胞(CTL)与同基因肿瘤细胞的相互作用,并将其与CTL-异基因肿瘤细胞相互作用进行了比较。本研究的主要结论如下:1)同基因和异基因CTL通过相似的机制裂解靶细胞。2)同基因系统中反应性降低是由于能够结合并杀死肿瘤细胞的效应细胞含量低。3)CTL-同基因肿瘤细胞结合的亲和力低于CTL-异基因肿瘤细胞结合。我们认为后两个观察结果是由于同基因宿主中肿瘤细胞的免疫原性低所致。