Okada M, Minamishima Y
Microbiol Immunol. 1987;31(1):45-57. doi: 10.1111/j.1348-0421.1987.tb03067.x.
The host-mediated antiviral effect of two biological response modifiers (BRM), OK-432 and PS-K, against murine cytomegalovirus (MCMV) was evaluated in normal and immunologically deficient mice of the same litters. In normal littermate mice, BALB/c (nu/+) or C57BL/6 (bg/+), the BRM-induced resistance against MCMV infection was evidenced by increase in fifty percent lethal doses, decrease in titers of viruses replicated in the target organs and augmentation of natural killer (NK) cell activity of the spleen cells. In T cell-deficient, athymic nude mice, BALB/c (nu/nu), the protective effect was manifested by prolongation of the survival, decrease in the virus titers, and increase in the NK-cell activity, but without decrease in mortality. In NK cell-deficient, beige mutant mice, C57BL/6 (bg/bg), the BRM-induced protection was nullified or minimized, and there was little difference in those parameters between BRM-treated and untreated mice. However, with higher doses of OK-432, but not PS-K, or with sublethal doses of MCMV, the NK cell activity was slightly augmented in the beige mutant mice. Thus both NK cell and T cell activity are essential for mice to overcome acute MCMV infection and it is likely that the protective effect of BRM manifests itself fully, at least in immunologically intact mice.
在同一窝的正常和免疫缺陷小鼠中评估了两种生物反应调节剂(BRM),即OK-432和PS-K,对小鼠巨细胞病毒(MCMV)的宿主介导抗病毒作用。在正常同窝小鼠,BALB/c(nu/+)或C57BL/6(bg/+)中,BRM诱导的抗MCMV感染抵抗力表现为半数致死剂量增加、靶器官中复制病毒的滴度降低以及脾细胞自然杀伤(NK)细胞活性增强。在T细胞缺陷的无胸腺裸鼠BALB/c(nu/nu)中,保护作用表现为生存期延长、病毒滴度降低以及NK细胞活性增加,但死亡率没有降低。在NK细胞缺陷的米色突变小鼠C57BL/6(bg/bg)中,BRM诱导的保护作用无效或最小化,BRM处理组和未处理组小鼠在这些参数上几乎没有差异。然而,使用更高剂量的OK-432而非PS-K,或使用亚致死剂量的MCMV时,米色突变小鼠的NK细胞活性略有增强。因此,NK细胞和T细胞活性对于小鼠克服急性MCMV感染都是必不可少的,并且BRM的保护作用可能至少在免疫健全的小鼠中充分显现。