Marino P A, Adams D O
J Immunol. 1982 Jun;128(6):2816-23.
The capacity for augmented binding of tumor cells is an initial and necessary part of macrophage-mediated tumor cytotoxicity. To study the induction of binding capacity, we obtained FCS-elicited, inflammatory macrophages from C57BL/6J mice. Exposure of these macrophages to lymphokine(s) containing MAF induced augmented binding capacity in a dose-dependent fashion. Resident peritoneal macrophages did not respond to lymphokine, and endotoxin did not appreciably influence induction of binding. Maximum induction of binding required continuous interaction between macrophages and lymphokine for 6 to 10 hr. The conditions necessary for induction of binding closely paralleled those for induction of priming or cytolysis. Exposure of FCS-elicited macrophages from C3H/HeJ mice, although not of macrophages from A/J mice, induced augmented binding. The data suggest that the augmented capacity for binding tumor cells is induced by lymphokine(s) and that a major part of induction of priming for cytolysis by MAF is induction of such binding.
肿瘤细胞增强结合能力是巨噬细胞介导的肿瘤细胞毒性的初始且必要的部分。为了研究结合能力的诱导过程,我们从C57BL/6J小鼠中获取了经FCS诱导产生的炎性巨噬细胞。将这些巨噬细胞暴露于含有巨噬细胞激活因子(MAF)的淋巴因子中,会以剂量依赖的方式诱导其增强结合能力。驻留腹膜巨噬细胞对淋巴因子无反应,内毒素对结合诱导也没有明显影响。结合的最大诱导需要巨噬细胞与淋巴因子持续相互作用6至10小时。诱导结合所需的条件与诱导启动或细胞溶解的条件密切平行。来自C3H/HeJ小鼠的经FCS诱导的巨噬细胞暴露后会诱导增强结合,而A/J小鼠的巨噬细胞则不会。数据表明,肿瘤细胞增强结合能力是由淋巴因子诱导的,并且MAF诱导细胞溶解启动的主要部分是这种结合的诱导。