CD4+ T cells and gamma interferon in the long-term control of persistent friend retrovirus infection
CD4+ T cells and gamma interferon in the long-term control of persistent friend retrovirus infection
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DOI：
10.1128/jvi.75.1.52-60.2001
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发表时间：
2001-01-01
影响因子：
5.4
通讯作者：
Hasenkrug, KJ
中科院分区：
文献类型：
--
作者：
Iwashiro, M;Peterson, K;Hasenkrug, KJ
我们使用Friend病毒模型来确定免疫系统控制持续逆转录病毒感染的基本机制。之前我们显示了CD4(+)T细胞在控制持续逆转录病毒方面发挥着重要作用，目前用Friend病毒特异性CD4(+)T细胞克隆进行的体外实验显示，这些细胞产生伽玛干扰素(IPN-伽马)，它具有两种不同的抗病毒活性机制。首先，干扰素-γ对病毒的产生有直接抑制作用。这种抑制作用是非细胞溶解的，有趣的是，这种抑制作用与细胞表面病毒抗原表达的减少无关。干扰素-γ介导的抗病毒活性的第二个机制是增强CD4(+)T细胞介导的细胞溶解活性。我们还发现了干扰素-γ在体内控制Friend病毒感染的作用，在持续感染的小鼠中中和干扰素-γ导致脾中病毒水平显著增加，并且很大比例的干扰素-γ缺陷小鼠无法保持对Friend病毒感染的长期控制。
We have used the Friend virus model to determine the basic mechanisms by which the immune system can control persistent retroviral infections. Previously we showed that CD4(+) T cells play an essential role in keeping persistent retrovirus in check, The present in vitro experiments with a Friend virus-specific CD4(+) T-cell clone revealed that these cells produce gamma interferon (IPN-gamma), which acts with two distinct mechanisms of antiviral activity. First, IFN-gamma had a direct inhibitory effect on virus production. This inhibitory effect was noncytolytic and, interestingly, was not associated with decreased cell surface expression of viral antigens. The second mechanism of IFN-gamma -mediated antiviral activity was an enhancement of CD4(+) T-cell-mediated cytolytic activity. We also found an in vivo role for IFN-gamma in the control of persistent Friend virus infections, Neutralization of IFN-gamma in persistently infected mice resulted in significantly increased levels of virus in the spleen, and a significant percentage of IFN-gamma -deficient mice were unable to maintain long-term control over Friend virus infections.