Surface expression of HLA-E, an inhibitor of natural killer cells, enhanced by human cytomegalovirus gpUL40
Surface expression of HLA-E, an inhibitor of natural killer cells, enhanced by human cytomegalovirus gpUL40
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DOI：
10.1126/science.287.5455.1031
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发表时间：
2000-02-11
期刊：
影响因子：
56.9
通讯作者：
Wilkinson, GWG
中科院分区：
文献类型：
--
作者：
Tomasec, P;Braud, VM;Wilkinson, GWG
非经典主要组织相容性复合体（MHC）I类分子HLA-E通过与CD 94/NKG 2A受体相互作用来抑制自然杀伤（NK）细胞介导的溶解。HLA-E的表面表达依赖于来自MHC I类分子的保守肽的结合。相同的肽存在于人巨细胞病毒（HCMV）糖蛋白UL 40（gpUL 40）的前导序列中。研究表明，与抗原加工相关的转运蛋白无关，gpUL 40可以上调HLA-E的表达，从而保护靶细胞免受NK细胞裂解。虽然经典的MHC I类分子被下调，但HLA-E被HCMV上调。gpUL 40诱导HLA-E表面表达可能代表HCMV逃逸途径。
The nonclassical major histocompatibility complex (MHC) class I molecule HLA-E inhibits natural killer (NK) cell-mediated lysis by interacting with CD94/ NKG2A receptors. Surface expression of HLA-E depends on binding of conserved peptides derived from MHC class I molecules. The same peptide is present in the leader sequence of the human cytomegalovirus (HCMV) glycoprotein UL40 (gpUL40). It is shown that, independently of the transporter associated with antigen processing, gpUL40 can up-regulate expression of HLA-E, which protects targets from NK cell Lysis. While classical MHC class I molecules are down-regulated, HLA-E is up-regulated by HCMV. induction of HLA-E surface expression by gpUL40 may represent an escape route for HCMV.