Reyburn H T, Mandelboim O, Valés-Gómez M, Davis D M, Pazmany L, Strominger J L
Department of Molecular and Cellular Biology, Harvard University, Cambridge, Massachusetts 02138, USA.
Nature. 1997 Apr 3;386(6624):514-7. doi: 10.1038/386514a0.
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.
I类主要组织相容性复合体（MHC）限制的细胞毒性T淋巴细胞（CTL）对病毒感染细胞的识别与破坏，是免疫系统控制和消除病毒感染努力的核心部分。因此，许多病毒已进化出干扰I类MHC分子上肽抗原加工与呈递的策略也就不足为奇了（参考文献1中有综述）。这些机制会阻止或减少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）。因此，任何为避免CTL攻击而失去I类MHC细胞表面表达的病毒感染细胞，都应易受NK细胞介导的破坏。据我们所知，我们在此描述了首个病毒逃避NK细胞免疫监视策略的例子。
