Germain R N, Williams R M, Benacerraf B
J Natl Cancer Inst. 1975 Mar;54(3):709-20.
The recently described inhibition of DNA synthesis (IDS) assay, which measures antitumor effector (E) cell function by the quantitation of decreases in tritiated thymidine incorporation of target tumor cells, was used to analyze the nonspecific effector activity of peritoneal exudate cells (PEC) from mice infected intraperitoneally with BCG. These PEC could inhibit growth of and then kill all tumor target (effector to target) cells tested at E/T ratios as low as 1:1. This activity was not due to alterations in media, nor could any activity be shown for cell-free supernatants prepared from active cells. The principal cell type mediating this effector function was the "activated" macrophage-no activity was found in lymphoid or polymorphonuclear leukocytes. Direct effector to target contact was necessary for the cytotoxic reaction. The time course of these effects and comparative 51Cr release data were reported. The removal of the adherent nonspecific effectors from PEC of mice immunized to both BCG and a specific syngeneic tumor revealed a specific cytotoxicity of the remaining lymphoid cells. These results indicated that nonspecific effector activity by "activated" macrophages induced by BCG infection could be a potent antitumor mechanism, at least in vitro, and the IDS assay provided an accurate, reproducible, and quantitative method for measurement of the function of such E cells.
最近描述的DNA合成抑制（IDS）试验，通过定量标记胸腺嘧啶核苷掺入靶肿瘤细胞的减少来测量抗肿瘤效应（E）细胞功能，用于分析经卡介苗腹腔感染的小鼠腹腔渗出细胞（PEC）的非特异性效应活性。这些PEC能在低至1:1的E/T比下抑制并随后杀死所有测试的肿瘤靶（效应细胞与靶细胞）细胞的生长。这种活性不是由于培养基的改变，从活性细胞制备的无细胞上清液也未显示出任何活性。介导这种效应功能的主要细胞类型是“活化的”巨噬细胞——在淋巴细胞或多形核白细胞中未发现活性。细胞毒性反应需要效应细胞与靶细胞直接接触。报告了这些效应的时间进程和比较性的51Cr释放数据。从同时免疫卡介苗和同基因特异性肿瘤的小鼠的PEC中去除黏附性非特异性效应细胞，揭示了剩余淋巴细胞的特异性细胞毒性。这些结果表明，卡介苗感染诱导的“活化”巨噬细胞的非特异性效应活性可能是一种有效的抗肿瘤机制，至少在体外是如此，并且IDS试验为测量此类E细胞的功能提供了一种准确、可重复和定量的方法。
