Scornik J C, Klein P A
J Natl Cancer Inst. 1978 Oct;61(4):1143-8.
Possible mechanisms of in vivo killing of tumor cells by antibody (Ab) were explored in a model in which Ab suppresses tumor growth in mice. A proportion of tumor cells injected into the peritoneal cavities of complement-deficient A/J mice was lysed within 30 minutes in the presence of anti-tumor cell Ab as demonstrated by the release of 51Cr in vivo. Experiments in which [125I]5-iodo-2'-deoxyuridine-labeled tumor cells were used showed that most tumor cells did not leave the injection site and that lysis occurred inside the peritoneal cavity. In addition, a proportion of the remaining sensitized tumor cells was significantly damaged, as shown by their decreased resistance to osmotic lysis. Morphologic studies ruled out phagocytosis of tumor cells as a mechanism of major significance. Tumor cell damage but not tumor cell lysis could also be induced in vitro with Ab and normal peritoneal cells. These results provided direct evidence of primary cytolysis induced by Ab in vivo, though other concomitant cytotoxic mechanisms may also take place in this model.
在一个抗体（Ab）抑制小鼠肿瘤生长的模型中，研究了抗体在体内杀伤肿瘤细胞的可能机制。将肿瘤细胞注入补体缺陷的A/J小鼠腹腔，在抗肿瘤细胞抗体存在的情况下，一部分肿瘤细胞在30分钟内被裂解，体内51Cr的释放证明了这一点。使用[125I]5-碘-2'-脱氧尿苷标记肿瘤细胞的实验表明，大多数肿瘤细胞没有离开注射部位，裂解发生在腹腔内。此外，其余一部分致敏肿瘤细胞受到显著损伤，表现为它们对渗透裂解的抵抗力下降。形态学研究排除了肿瘤细胞吞噬作为主要意义机制的可能性。抗体和正常腹腔细胞在体外也可诱导肿瘤细胞损伤，但不能诱导肿瘤细胞裂解。这些结果提供了抗体在体内诱导原发性细胞溶解的直接证据，尽管在该模型中可能也存在其他伴随的细胞毒性机制。
