The class I MHC homologue of human cytomegalovirus inhibits attack by natural killer cells
The class I MHC homologue of human cytomegalovirus inhibits attack by natural killer cells
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DOI：
10.1038/386514a0
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发表时间：
1997-04-03
期刊：
影响因子：
64.8
通讯作者：
Strominger, JL
中科院分区：
文献类型：
--
作者：
Reyburn, HT;Mandelboim, O;Strominger, JL
一类主要组织相容性复合体（MHC）限制性细胞毒性T淋巴细胞（CTL）识别和破坏病毒感染的细胞是免疫系统控制和消除病毒感染的核心部分。因此，毫不奇怪，许多病毒已经进化出了干扰I类MHC分子上肽抗原的加工和呈递的策略（参见文献1）。这些机制的作用是防止或减少MHC分子在细胞表面的表达。然而，许多自然杀伤（NK）细胞能够识别并破坏不再表达I类MHC分子的宿主细胞（“缺失自我”假说(2)）。因此，任何为避免CTL攻击而失去MHC I类细胞表面表达的病毒感染细胞，都应该容易受到nk细胞介导的破坏。我们在这里描述第一个例子，据我们所知，病毒策略逃避NK细胞的免疫监视。
Recognition and destruction of virus-infected cells by class I major histocompatibility complex (MHC) restricted cytotoxic T lymphocytes (CTL) is a central part of the immune system's attempts to control and eliminate virus infection. It is therefore not surprising that many viruses have evolved strategies to interfere with the processing and presentation of peptide antigen on class I MHC molecules (reviewed in ref. 1). These mechanisms act to prevent or reduce expression of MHC molecules at the cell surface. However, many natural killer (NK) cells are able to recognize and destroy host cells that no longer express class I MHC molecules (the 'missing self' hypothesis(2)). Thus, any virus-infected cell that has lost cell-surface expression of MHC class I to avoid CTL attack should become susceptible to NK-cell-mediated destruction. We describe here the first example, to our knowledge, of a viral strategy to evade immune surveillance by NK cells.