Adams D O, Pike M C, Snyderman R
J Immunol. 1981 Jul;127(1):225-30.
The ability of BCG-activated macrophages from C57BL/6J mice to lyse neoplastic targets was depressed by inhibitors of methyltransferase reactions (10(-4) M adenosine, 10(-5) M EHNA, and 10(-4) M L-homocysteine or 10(-5) M DZA). Binding of P815 mastocytoma targets to BCG-activated macrophages, which has been shown to be a necessary event in cytolysis of those targets, was also inhibited by adenosine, EHNA, and L-homocysteine or by DZA at the above concentrations. Inhibition of binding was obtained when macrophages were pretreated with the inhibitors, whereas pretreatment of targets with the inhibitors did not alter binding. The inhibitors were not toxic to the macrophages, as judged by morphology and viability of the macrophage cultures as well as by ability of macrophages to bind antibody-coated P815 targets or to secrete plasminogen activator. The inhibitors, at concentrations that inhibited cytolysis and binding, also depressed one type of S-adenosyl-L-methionine-mediated methylation reaction (protein carboxy-O-methylation) in BCG macrophages. The data suggest that transmethylation reactions are essential for the ability of BCG activated murine macrophages to bind and, hence, to destroy P815 tumor cells.
来自C57BL/6J小鼠的卡介苗激活巨噬细胞溶解肿瘤靶标的能力受到甲基转移酶反应抑制剂（10⁻⁴ M腺苷、10⁻⁵ M EHNA、10⁻⁴ M L-高半胱氨酸或10⁻⁵ M DZA）的抑制。P815肥大细胞瘤靶标与卡介苗激活巨噬细胞的结合，已被证明是这些靶标细胞溶解过程中的一个必要事件，也受到上述浓度的腺苷、EHNA、L-高半胱氨酸或DZA的抑制。当巨噬细胞用抑制剂预处理时可获得结合抑制，而用抑制剂预处理靶标则不会改变结合。从巨噬细胞培养物的形态和活力以及巨噬细胞结合抗体包被的P815靶标或分泌纤溶酶原激活剂的能力判断，这些抑制剂对巨噬细胞无毒。在抑制细胞溶解和结合的浓度下，这些抑制剂也降低了卡介苗巨噬细胞中一种S-腺苷-L-甲硫氨酸介导的甲基化反应（蛋白质羧基-O-甲基化）。数据表明，转甲基化反应对于卡介苗激活的小鼠巨噬细胞结合并因此破坏P815肿瘤细胞的能力至关重要。
