Shimada S, Yano O, Tokunaga T
Jpn J Cancer Res. 1986 Aug;77(8):808-16.
A fraction extracted from BCG and designated MY-1, which was composed of 70.0% DNA and 28.0% RNA, was previously reported to possess strong antitumor activities against various syngeneic mouse and guinea pig tumors. An intraperitoneal injection of MY-1 (100 micrograms) 1 day before rendered mouse peritoneal cells cytotoxic to YAC-1 cells. The effector cells were nonadherent to plastic dishes, and the activity was destroyed by treatment with anti-asialo GM1 antiserum plus complement or carrageenan in vitro, but not with carbonyl-iron or anti-Thy 1.2, suggesting that the cells are natural killer (NK) cells. In vivo augmentation of NK activity was dependent on MY-1 dose, and reached the peak 1 day after MY-1 injection. Since NK activity in lipopolysaccharide (LPS)-nonresponder mice could be augmented by MY-1, the possibility that LPS contaminated the MY-1-augmented NK was excluded. MY-1 digested preliminarily with DNase lost its NK-inducing activity, suggesting that the DNA entity of MY-1 was essential for the activity. When mice were pretreated with anti-asialo GM1 or carrageenan, MY-1 could not render the peritoneal cells cytotoxic. Antitumor activities of MY-1 were also abolished if the animals were pretreated with anti-asialo GM1 antiserum or carrageenan, suggesting that the activities can be ascribed mainly to activated NK cells.
一种从卡介苗中提取的名为MY-1的组分,其由70.0%的DNA和28.0%的RNA组成,此前有报道称它对多种同基因小鼠和豚鼠肿瘤具有强大的抗肿瘤活性。在给小鼠腹腔注射YAC-1细胞前1天腹腔注射MY-1(100微克),可使小鼠腹腔细胞对YAC-1细胞产生细胞毒性。效应细胞不黏附于塑料培养皿,其活性在体外经抗去唾液酸GM1抗血清加补体或角叉菜胶处理后被破坏,但经羰基铁或抗Thy 1.2处理则不受影响,这表明这些细胞是自然杀伤(NK)细胞。体内NK活性的增强依赖于MY-1的剂量,并在注射MY-1后1天达到峰值。由于MY-1可增强脂多糖(LPS)无反应小鼠的NK活性,因此排除了LPS污染MY-1增强的NK的可能性。经DNase初步消化的MY-1失去了其诱导NK的活性,这表明MY-1的DNA实体对该活性至关重要。当用抗去唾液酸GM1或角叉菜胶预处理小鼠时,MY-1不能使腹腔细胞产生细胞毒性。如果用抗去唾液酸GM1抗血清或角叉菜胶预处理动物,MY-1的抗肿瘤活性也会被消除,这表明这些活性主要可归因于活化的NK细胞。