KIR2DL4 拷贝数变异与 SIV 感染的 Mamu-A*01 阴性恒河猴中 CD4+ T 细胞耗竭和细胞因子产生 NK 细胞亚群的功能有关。
KIR2DL4 copy number variation is associated with CD4+ T-cell depletion and function of cytokine-producing NK cell subsets in SIV-infected Mamu-A*01-negative rhesus macaques.
机构信息
Center for Virology and Vaccine Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
出版信息
J Virol. 2013 May;87(9):5305-10. doi: 10.1128/JVI.02949-12. Epub 2013 Feb 28.
Abstract
Here, we demonstrate that KIR2DL4 copy number variation (CNV) is associated with CD4(+) T-cell decline and functionality of cytokine-producing NK cells during primary simian immunodeficiency virus (SIV) infection in Mamu-A*01(-) Indian-origin rhesus macaques, with higher KIR2DL4 copy numbers being associated with a better preservation of CD4(+) T cells and an increased gamma interferon (IFN-γ) production from stimulated cytokine-producing NK cell subsets during acute SIVmac251 infection. These findings underscore the crucial role of activating killer-cell immunoglobulin-like receptors (KIRs) in NK cell-mediated SIV responses during early SIV infection.
摘要
在这里，我们证明了在 Mamu-A*01(-)印度起源的恒河猴中，KIR2DL4 拷贝数变异 (CNV) 与原发性猴免疫缺陷病毒 (SIV) 感染期间的 CD4(+) T 细胞减少和细胞因子产生的 NK 细胞功能有关，较高的 KIR2DL4 拷贝数与更好地保存 CD4(+) T 细胞有关，并在急性 SIVmac251 感染期间增加刺激细胞因子产生的 NK 细胞亚群中产生γ干扰素 (IFN-γ)。这些发现强调了在早期 SIV 感染期间，激活杀伤细胞免疫球蛋白样受体 (KIR) 在 NK 细胞介导的 SIV 反应中的关键作用。
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