Marino P A, Whisnant C C, Adams D O
J Exp Med. 1981 Jul 1;154(1):77-87. doi: 10.1084/jem.154.1.77.
The binding of tumor cells by activated macrophages is an initial and necessary event in the cytolysis of these targets. The data here indicate that membrane preparations from RL sigma 1 leukemia targets, EL-4 lymphoma targets, and P815 mastocytoma targets each inhibited binding of its homologous target to bacillus Calmette-Guérin (BCG)-activated murine macrophages in a dose-dependent fashion. Similar amounts of membrane from lymphocytes did not alter binding of the three neoplastic target to BCG-macrophages. Membranes of the three targets also inhibited binding of the heterologous neoplastic targets. Inhibitory activity of membrane preparations from P815, EL-4, and RL sigma 1 targets could be adsorbed by incubation of limiting concentrations of the membrane preparations with BCG-activated macrophages but not with thioglycollate broth-elicited macrophages. Exposure of BCG macrophages to membrane preparations from RL sigma 1, FL-4, or P815 targets inhibited subsequent cytolysis of the three targets. Inhibitory activity was increased in preparations enriched for plasma membrane. The data suggest that binding of three murine, nonadherent neoplastic targets to BCG-activated murine macrophages is mediated, in part, by recognition structures present within the plasma membranes of the three targets.
活化巨噬细胞对肿瘤细胞的结合是这些靶细胞溶解过程中的一个初始且必要的事件。此处的数据表明,来自RL sigma 1白血病靶细胞、EL-4淋巴瘤靶细胞和P815肥大细胞瘤靶细胞的膜制剂均以剂量依赖的方式抑制其同源靶细胞与卡介苗(BCG)活化的小鼠巨噬细胞的结合。相似量的淋巴细胞膜并未改变这三种肿瘤靶细胞与BCG巨噬细胞的结合。这三种靶细胞的膜也抑制异源肿瘤靶细胞的结合。通过将有限浓度的P815、EL-4和RL sigma 1靶细胞膜制剂与BCG活化的巨噬细胞共同孵育,而非与巯基乙酸肉汤诱导的巨噬细胞共同孵育,可吸附其抑制活性。将BCG巨噬细胞暴露于来自RL sigma 1、FL-4或P815靶细胞的膜制剂会抑制随后对这三种靶细胞的溶解。富含质膜的制剂中抑制活性增强。数据表明,三种小鼠非贴壁肿瘤靶细胞与BCG活化的小鼠巨噬细胞的结合部分是由这三种靶细胞质膜内存在的识别结构介导的。