Soldateschi D, Boraschi D, Tagliabue A
Antiviral Res. 1985 Aug;5(4):217-27. doi: 10.1016/0166-3542(85)90026-9.
Resident mouse peritoneal cells (PC) express a significant antiviral activity against encephalomyocarditis virus (EMCV) in vitro, as judged by decreased virus yield from infected mouse embryo fibroblasts (MEF). This natural antiviral activity of PC was not due either to enhanced lysis of virus-infected cells, as these were protected from lysis rather than destructed by PC, or to interferon (IFN) production, as no direct correlation between IFN and anti-EMCV activity was found. Among PC, macrophages (M phi) appear to be responsible for the anti-EMCV activity, which was indeed attributable to a Thy 1.2-negative, adherent mononuclear cell. Moreover, M phi-defective C3H/HeJ mice showed a significant impairment of anti-EMCV activity, whereas M phi of mice defective for natural killer (NK) activity (bg/bg, SJL/J) or for mature T cells (nu/nu) possessed an intact antiviral capacity.
通过感染的小鼠胚胎成纤维细胞(MEF)病毒产量降低判断,驻留小鼠腹膜细胞(PC)在体外对脑心肌炎病毒(EMCV)表现出显著的抗病毒活性。PC的这种天然抗病毒活性既不是由于病毒感染细胞的裂解增强,因为这些细胞受到保护而未被PC裂解,也不是由于干扰素(IFN)产生,因为未发现IFN与抗EMCV活性之间存在直接相关性。在PC中,巨噬细胞(M phi)似乎负责抗EMCV活性,这实际上归因于Thy 1.2阴性的贴壁单核细胞。此外,M phi缺陷的C3H/HeJ小鼠表现出抗EMCV活性的显著受损,而天然杀伤(NK)活性缺陷(bg/bg,SJL/J)或成熟T细胞缺陷(nu/nu)的小鼠的M phi具有完整的抗病毒能力。