Mackewicz C E, Ortega H, Levy J A
Cancer Research Institute, University of California, School of Medicine, San Francisco 94143-0128.
Cell Immunol. 1994 Feb;153(2):329-43. doi: 10.1006/cimm.1994.1032.
CD8+ cells from HIV-infected individuals inhibit HIV replication in cultured CD4+ cells by a nonlytic, non-MHC-restricted mechanism. The activity appears to be mediated in part by a soluble antiviral factor (CAF) secreted by the CD8+ cells. In an attempt to identify this factor a large panel of recombinant cytokines was examined for their effect on HIV replication in CD4+ cells. In addition to interferon-alpha and -beta, TNF alpha, TGF beta, and IL-8 reduced virus replication in a dose-dependent fashion. In some cases, the effect of the cytokine was also dependent on the HIV infection assay used to measure it. Antibodies against the inhibitory cytokines, as well as antibodies against TNF beta, IFN-alpha, IFN-beta, IL-4, and IL-6 did not inactivate the antiviral effect of CAF. The data suggest that CAF does not have identity with known antiviral cytokines and therefore CAF may be a novel antiviral factor.
来自HIV感染者的CD8+细胞通过一种非裂解性、非MHC限制的机制抑制培养的CD4+细胞中的HIV复制。这种活性似乎部分由CD8+细胞分泌的一种可溶性抗病毒因子(CAF)介导。为了鉴定这种因子,检测了一大组重组细胞因子对CD4+细胞中HIV复制的影响。除了干扰素-α和-β外,肿瘤坏死因子-α、转化生长因子-β和白细胞介素-8以剂量依赖的方式降低了病毒复制。在某些情况下,细胞因子的作用还取决于用于测量它的HIV感染检测方法。针对抑制性细胞因子的抗体,以及针对肿瘤坏死因子-β、干扰素-α、干扰素-β、白细胞介素-4和白细胞介素-6的抗体,均未使CAF的抗病毒作用失活。数据表明,CAF与已知的抗病毒细胞因子不同,因此CAF可能是一种新型抗病毒因子。