Matsubara S, Suzuki M, Ishida N
Cancer Res. 1980 Mar;40(3):873-6.
The response of mice to type II interferon inducers such as purified protein derivative of tuberculin or OK-432 was significantly impaired after either the implantation of tumor cells or the injection of cell-free tumor ascitic fluids. Complete inhibition of type II interferon induction occurred in 3 to 5 days. This inhibitory effect persisted until the death of mice implanted with tumors or for 7 days after i.p. injection of 0.2 ml of tumor ascitic fluid. The inhibitory activity was seen even with 0.2 ml of the 10,000-fold dilution of the fluid and with its filtrate passed through a Diaflo UM-10 membrane (greater than 10,000-dalton exclusion), However, such tumor ascitic fluids did not affect the induction of type I interferon in mice by polyriboinosinic-polyribocytidylic acid or tilorone-HCl. Moreover, adjuvant-induced nontumorous ascitic fluid had no inhibitory activity. These results indicate that the in vivo induction of type II interferon is specifically impaired by tumor-mediated factor(s) with molecular weights of less than 10,000.
在植入肿瘤细胞或注射无细胞肿瘤腹水后，小鼠对结核菌素纯蛋白衍生物或OK-432等II型干扰素诱导剂的反应显著受损。3至5天内完全抑制了II型干扰素的诱导。这种抑制作用一直持续到植入肿瘤的小鼠死亡，或在腹腔注射0.2 ml肿瘤腹水后持续7天。即使是0.2 ml经10000倍稀释的腹水及其通过Diaflo UM-10膜（截留分子量大于10000道尔顿）过滤后的滤液，也能观察到抑制活性。然而，这种肿瘤腹水并不影响聚肌苷酸-聚胞苷酸或盐酸泰洛龙在小鼠体内诱导I型干扰素。此外，佐剂诱导的非肿瘤性腹水没有抑制活性。这些结果表明，肿瘤介导的分子量小于10000的因子可特异性损害II型干扰素的体内诱导。
