CD4+自然杀伤细胞可被HIV有效感染，导致CD4表达下调和功能改变。
CD4+ NK cells can be productively infected with HIV, leading to downregulation of CD4 expression and changes in function.
作者信息
Bernstein Helene B, Wang Guangwu, Plasterer Mary C, Zack Jerome A, Ramasastry Parthasarathy, Mumenthaler Shannon M, Kitchen Christina M R
机构信息
Department of Reproductive Biology, Case Western Reserve University School of Medicine, Cleveland, OH, USA.
出版信息
Virology. 2009 Apr 25;387(1):59-66. doi: 10.1016/j.virol.2009.01.044. Epub 2009 Feb 28.
NK cells mediate the innate immune response, and HIV-infected individuals demonstrate altered NK cell phenotype and function. We find that CD4+ NK cells are susceptible to HIV infection; this could account for the NK cell dysfunction seen in HIV-infected individuals. CD4+ NK cells express CXCR4 and can be infected with X4-tropic viruses and some primary R5-utilizing viral isolates. Treatment with the CXCR4 ligands AMD3100 and SDF-1alpha partially blocks infection with X4-tropic virus, treatment with anti-CCL Igs upregulates CCR5 surface expression and enables infection with HIV-Bal. HIV infection of NK cells results in CD4 downregulation and the production of infectious virus. HIV-infected CD4+ NK cells mediate NK cell cytotoxicity, however, HIV infection is associated with decreased chemotaxis towards IL-16. Thus, HIV infection of CD4+ NK cells could account for the NK cell dysfunction observed in HIV-infected individuals. Furthermore infected NK cells could serve as a viral reservoir of HIV in vivo.
自然杀伤细胞介导先天性免疫反应，而感染HIV的个体表现出自然杀伤细胞表型和功能的改变。我们发现CD4⁺自然杀伤细胞易受HIV感染；这可能解释了在感染HIV的个体中观察到的自然杀伤细胞功能障碍。CD4⁺自然杀伤细胞表达CXCR4，可被X4嗜性病毒和一些利用R5的原发性病毒分离株感染。用CXCR4配体AMD3100和SDF-1α处理可部分阻断X4嗜性病毒的感染，用抗CCL免疫球蛋白处理可上调CCR5表面表达并使细胞能够被HIV-Bal感染。自然杀伤细胞感染HIV会导致CD4下调并产生传染性病毒。感染HIV的CD4⁺自然杀伤细胞介导自然杀伤细胞的细胞毒性，然而，HIV感染与对IL-16的趋化性降低有关。因此，CD4⁺自然杀伤细胞感染HIV可能解释了在感染HIV的个体中观察到的自然杀伤细胞功能障碍。此外，受感染的自然杀伤细胞可能在体内充当HIV的病毒储存库。
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