JLB：武汉大学发现抗艾滋病毒感染新细胞

武汉大学基础医学院侯炜教授和武汉大学动物实验中心科研人员合作的一项科研成果发表在8月份美国著名国际学术刊物《淋巴细胞生物学》杂志上。这项研究发现，一种名为“表达CD56分子的T淋巴细胞”具有抗艾滋病毒感染的作用。

据侯炜教授介绍，这种名为“表达CD56分子的T淋巴细胞”是一类“桥梁细胞”，既具有自然杀伤功能，又能起到自我保护作用。它是人类天然免疫系统的一个重要的组成部分，在外周血单核细胞中占5%-15%，而肠道和肝脏中的50%免疫细胞为“表达CD56分子的T淋巴细胞”。此前研究只被发现这种细胞在抗肿瘤和抗肝炎病毒感染中起作用，而没有发现它在抗艾滋病毒感染有较强作用。

侯炜教授和武汉大学动物实验中心霍文哲教授团队历经3年多研究，首次发现“表达CD56分子的T淋巴细胞”培养液中的分泌物可以抑制艾滋病毒的感染和复制，并且这种活性具有广谱性，既可抑制实验室保存的艾滋病毒病毒株，也可抑制临床上分离得到的艾滋病毒病毒株。

这个研究团队发现，虽然该培养液中的分泌物对艾滋病毒进入细胞的协同受体影响甚微，但可增强干扰素调节因子的作用，从而引起巨噬细胞发挥作用，“抗击”艾滋病毒。

doi: 10.1189/jlb.0312146

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CD56+ T cells inhibit HIV-1 infection of macrophages

Wei Hou, Li Ye and Wen-Zhe Ho

CD56+ T cells, the crucial component of the host innate immune system, play an important role in defense against viral infections. We investigated the noncytolytic anti-HIV-1 activity of primary CD56+ T cells. SNs collected from CD56+ T cell cultures inhibited HIV-1 infection and replication. This CD56+ T SN-mediated anti-HIV-1 activity was broad-spectrum, as CD56+ T SNs could inhibit infections by laboratory-adapted and clinical strains of HIV-1. The antibody to IFN-γ could partially block the CD56+ T SN-mediated anti-HIV effect. Investigation of mechanism(s) of the CD56+ T cell action on HIV-1 showed that although CD56+ T SN had little effect on HIV-1 entry coreceptor CCR5 expression, CD56+ T SN induced the expression of CC-chemokines, the ligands for CCR5. The antibodies to CC-chemokines also significantly blocked CD56+ T SN-mediated anti-HIV activity. Furthermore, CD56+ T SN up-regulated the expression of STAT-1/-2 and enhanced the expression of IRF1, -3, -7, and -9, resulting in the induction of endogenous IFN-α/β expression in macrophages. Moreover, CD56+ T SN up-regulated intracellular expression of APOBEC3G/3F, the recently identified HIV-1 restriction factors. These findings provide compelling evidence that CD56+ T cells may have a critical role in innate immunity against HIV-1 infection.