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The class I MHC homologue of human cytomegalovirus inhibits attack by natural killer cells

机译:人类巨细胞病毒的I类MHC同源物抑制自然杀伤细胞的攻击

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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). 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.
机译:I类主要组织相容性复合物(MHC)限制的细胞毒性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重要组成部分。因此,不足为奇的是,许多病毒已经进化出策略来干扰I类MHC分子上肽抗原的加工和呈递(参见参考文献1)。这些机制可防止或减少MHC分子在细胞表面的表达。但是,许多自然杀伤(NK)细胞能够识别和破坏不再表达I类MHC分子的宿主细胞(“自我缺失”假设)。因此,任何丢失了I类MHC细胞表面表达以避免CTL攻击的病毒感染细胞都应该易于受到NK细胞介导的破坏。据我们所知,我们在这里描述了第一个例子,该例子说明了一种通过NK细胞逃避免疫监视的病毒策略。

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