Expression of ICP0 is sufficient to trigger natural killer cell recognition of herpes simplex virus-infected cells by natural cytotoxicity receptors
Expression of ICP0 is sufficient to trigger natural killer cell recognition of herpes simplex virus-infected cells by natural cytotoxicity receptors
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DOI：
10.1086/512862
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发表时间：
2007-04-15
影响因子：
6.4
通讯作者：
Reyburn, Hugh T.
中科院分区：
文献类型：
--
作者：
Chisholm, Susan E.;Howard, Keith;Reyburn, Hugh T.
自然杀伤（NK）细胞是对许多病毒的免疫反应的重要组成部分;然而，NK细胞如何区分健康细胞和病毒感染细胞的分子基础在很大程度上是未知的。在这里，我们表明，立即早期基因产物ICP 0的表达足以产生增加的易感性，单纯疱疹病毒（HSV）感染的细胞的NK细胞裂解。该效应不依赖于主要组织相容性复合物I类分子的下调或活化NKG 2D受体配体表达的诱导。NK细胞对HSV ICP 0基因表达诱导的靶细胞变化的检测取决于天然细胞毒性受体（NCR）NKp 30、NKp 44和NKp 46。据我们所知，这是第一次鉴定出一种病毒基因，该基因触发NCR的细胞配体的上调;此外，这些观察结果突出了NCR对NK细胞对病毒感染的免疫监视的重要性。
Natural killer (NK) cells are an important component of the immune response to a number of viruses; however, the molecular basis of how NK cells discriminate between healthy and virus-infected cells is largely unknown. Here, we show that expression of the immediate-early gene product ICP0 is sufficient to produce an increased susceptibility to NK lysis of herpes simplex virus (HSV)-infected cells. This effect does not depend on downregulation of major histocompatibility complex class I molecules or on the induction of expression of ligands for the activating NKG2D receptor. Detection by NK cells of the changes in the target cell induced by HSV ICP0 gene expression depends on the natural cytotoxicity receptors (NCRs) NKp30, NKp44, and NKp46. To our knowledge, this is the first identification of a viral gene that triggers the up-regulation of cellular ligands for the NCR; moreover, these observations highlight the importance of the NCR for immunosurveillance of viral infection by NK cells.