Sarzotti M, Gomes M da P, Hoffman P M
Retrovirus Research Center, Veterans Affairs Medical Center, Baltimore, School of Medicine, Maryland.
Viral Immunol. 1993 Fall;6(3):207-17. doi: 10.1089/vim.1993.6.207.
T cell-mediated production of IFN-gamma followed infection of adult, but not neonatal NFS/N mice with Cas-Br-M murine leukemia virus (Cas). The IFN-gamma response was associated with the appearance of CTL specific for Cas and with age-dependent resistance to neurologic disease. While both immune responses were mediated by a CD8-enriched population of T cells, IFN-gamma did not play a role in the activation of the Cas-specific CTL response. However, when given exogenously, IFN-gamma delayed the onset and reduced the incidence of Cas-induced neurologic disease. These data suggest that the IFN-gamma response to Cas infection may be an important host defense mechanism whose effects on virus replication and neurologic disease expression are independent of its effect on Cas-specific CTL.
在用Cas-Br-M鼠白血病病毒（Cas）感染成年而非新生的NFS/N小鼠后，T细胞介导产生γ干扰素（IFN-γ）。IFN-γ反应与针对Cas的细胞毒性T淋巴细胞（CTL）的出现以及对神经系统疾病的年龄依赖性抗性相关。虽然这两种免疫反应均由富含CD8的T细胞群体介导，但IFN-γ在Cas特异性CTL反应的激活中不起作用。然而，当外源性给予IFN-γ时，它会延迟Cas诱导的神经系统疾病的发作并降低其发生率。这些数据表明，对Cas感染的IFN-γ反应可能是一种重要的宿主防御机制，其对病毒复制和神经系统疾病表达的影响独立于其对Cas特异性CTL的影响。
