NK cell activation by KIR-binding antibody 1-7F9 and response to HIV-infected autologous cells in viremic and controller HIV-infected patients
NK cell activation by KIR-binding antibody 1-7F9 and response to HIV-infected autologous cells in viremic and controller HIV-infected patients
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DOI：
10.1016/j.clim.2009.10.001
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发表时间：
2010-02-01
影响因子：
8.6
通讯作者：
Berg, Louise
中科院分区：
文献类型：
--
作者：
Johansson, Susanne E.;Hejdeman, Bo;Berg, Louise
自然杀伤细胞（NK）可能在HIV感染中具有保护作用，并被杀伤细胞免疫球蛋白样受体（KIRs）与MHC I类分子（包括HLA-C）相互作用所抑制。在体外实验中，尽管HIV感染细胞上其他MHC I类分子下调，但HLA-C的保留可能保护感染细胞免受NK细胞的识别。为了评估抑制HLA-C配体在NK细胞识别自身感染T细胞能力中的作用，我们在体外测量了病毒血症患者、低病毒血症控制者和健康供者的NK细胞脱颗粒。与HIV-1（IIIB）感染目标相比，NK细胞对未感染目标的反应没有差异。NK细胞的活化受KIR的调控，因为NK细胞的脱颗粒被1-7F9（一种结合KIR2DL1/L2/L3和KIR2DS1/S2的人抗体）增加，这种作用在KIR单倍型B个体中最为明显。(C) 2009爱思唯尔公司版权所有。
Natural killer (NK) cells may be protective in HIV infection and are inhibited by killer cell immunoglobulin-like receptors (KIRs) interacting with MHC class I molecules, including HLA-C. Retention of HLA-C despite downregulation of other MHC class I molecules on HIV infected cells might protect infected cells from NK cell recognition in vitro. To assess the role of inhibitory HLA-C ligands in the capacity of NK cells to recognize autologous infected T cells, we measured NK cell degranulation in vitro in viremic patients, controllers with low viremia, and healthy donors. No difference in NK cell response to uninfected compared to HIV-1(IIIB) infected targets was observed. Activation of NK cells was regulated by KIRs, because NK cell degranulation was increased by 1-7F9, a human antibody that binds KIR2DL1/L2/L3 and KIR2DS1/S2, and this effect was most pronounced in KIR haplotype B individuals. (C) 2009 Elsevier Inc. All rights reserved.