Somers S D, Mastin J P, Adams D O
J Immunol. 1983 Oct;131(4):2086-93.
Peritoneal macrophages from C57BL/6N mice infected with BCG have a greater capacity for tumor cell binding than do inflammatory macrophages elicited by several agents. To determine if these quantitatively distinct types of binding were qualitatively distinct as well, we compared them in several ways. Scanning electron microscopy of macrophage-tumor cell interactions reveals clustering of 2 to 5 tumor targets on the central portion of BCG-activated macrophages, in contrast to the very few tumor cells found at the periphery of inflammatory macrophages. Tumor cell binding to BCG-activated macrophages required divalent cations and trypsin-sensitive surface structures on the macrophages, but the low-level binding to inflammatory macrophages required neither. The ability of trypsinized BCG-activated macrophages to bind P815 tumor targets was recovered with time in culture. BCG-activated macrophages required intact energy metabolism, microfilaments, and microtubules to complete augmented tumor cell binding, whereas inflammatory macrophages did not. Targets bound to BCG macrophages could be competitively removed by addition of large excesses of unlabeled tumor cells, but targets bound to inflammatory macrophages could not be so removed. Tumor cells labeled with 111Indium oxine were used to estimate the specific (i.e., competitively inhibitable) and nonspecific (noncompetitively inhibitable) components of binding. Binding of P815 tumor cells to BCG-activated macrophages was predominantly specific, whereas their binding to inflammatory macrophages was predominantly nonspecific. Binding by activated or inflammatory macrophages of lymphocytes or by transformed 3T3 cells of neoplastic or non-neoplastic targets was also nonspecific. Binding by BCG-elicited macrophages from A/J mice, previously demonstrated to be quantitatively deficient in binding ability, was qualitatively similar to that to inflammatory macrophages and was not competitively inhibitable. The data suggest that tumor cell binding by activated macrophages is qualitatively as well as quantitatively distinct from binding to inflammatory macrophages.
感染卡介苗的C57BL/6N小鼠的腹腔巨噬细胞比几种因子诱导产生的炎性巨噬细胞具有更强的肿瘤细胞结合能力。为了确定这些在数量上不同的结合类型在质量上是否也不同，我们从几个方面对它们进行了比较。巨噬细胞与肿瘤细胞相互作用的扫描电子显微镜显示，卡介苗激活的巨噬细胞中央部分聚集着2到5个肿瘤靶点，而炎性巨噬细胞周边几乎没有肿瘤细胞。肿瘤细胞与卡介苗激活的巨噬细胞结合需要二价阳离子和巨噬细胞表面对胰蛋白酶敏感的结构，但与炎性巨噬细胞的低水平结合则两者均不需要。胰蛋白酶处理过的卡介苗激活的巨噬细胞结合P815肿瘤靶点的能力会随着培养时间的延长而恢复。卡介苗激活的巨噬细胞需要完整的能量代谢、微丝和微管来完成增强的肿瘤细胞结合，而炎性巨噬细胞则不需要。与卡介苗巨噬细胞结合的靶点可以通过加入大量未标记的肿瘤细胞而被竞争性去除，但与炎性巨噬细胞结合的靶点则不能这样被去除。用111铟氧嗪标记的肿瘤细胞来估计结合的特异性（即可竞争性抑制的）和非特异性（非竞争性抑制的）成分。P815肿瘤细胞与卡介苗激活的巨噬细胞的结合主要是特异性的，而它们与炎性巨噬细胞的结合主要是非特异性的。激活的或炎性巨噬细胞对淋巴细胞的结合，或转化的3T3细胞对肿瘤或非肿瘤靶点的结合也是非特异性的。先前已证明A/J小鼠的卡介苗诱导的巨噬细胞在结合能力上数量不足，其结合在质量上与炎性巨噬细胞相似，且不可竞争性抑制。数据表明，激活的巨噬细胞对肿瘤细胞的结合在质量和数量上都与炎性巨噬细胞的结合不同。
