Langlois A J, Matthews T J, Weinhold K J, Bolognesi D P
J Natl Cancer Inst. 1985 Oct;75(4):709-15.
The mechanism by which IgG2A from a syngeneic antitumor hyperimmune serum mediates destruction of target cells in the presence of thioglycollate-elicited peritoneal macrophages was investigated by using an in vitro assay system. Labeled tumor cells were found to exhibit a biphasic pattern of binding to the effector cells; this binding pattern was dependent on the presence of specific antibody. The initial binding phase produced no apparent changes in the target cell population. Target cells coated with specific antibody exhibited a similar early binding phase, but excess free antibody was required for the subsequent binding phase and its associated release of radiolabel and cell destruction. Several features of this process observed distinguished it from more conventional forms of antibody-dependent cell-mediated cytoxicity. These included 1) the preference for antibodies of the IgG2A isotype, 2) the association of cell destruction with the release of nuclear but not cytoplasmic label, and 3) the requirement of excess free antibody for target cell killing.
通过使用体外分析系统,研究了来自同基因抗肿瘤超免疫血清的IgG2A在巯基乙酸盐诱导的腹腔巨噬细胞存在下介导靶细胞破坏的机制。发现标记的肿瘤细胞与效应细胞呈现双相结合模式;这种结合模式依赖于特异性抗体的存在。初始结合阶段在靶细胞群体中未产生明显变化。用特异性抗体包被的靶细胞表现出类似的早期结合阶段,但随后的结合阶段及其相关的放射性标记释放和细胞破坏需要过量的游离抗体。观察到该过程的几个特征使其有别于更传统形式的抗体依赖性细胞介导的细胞毒性。这些特征包括:1)对IgG2A同种型抗体的偏好;2)细胞破坏与细胞核而非细胞质标记物的释放相关;3)靶细胞杀伤需要过量的游离抗体。