Antoniou Antony N, Powis Simon J
Department of Immunology & Molecular Pathology, Division of Infection & Immunity, University College London, Windeyer Institute of Medical Science, London, UK.
Immunology. 2008 May;124(1):1-12. doi: 10.1111/j.1365-2567.2008.02804.x. Epub 2008 Feb 18.
Major histocompatibility complex (MHC) class I molecules bind and present short antigenic peptides from endogenously or exogenously derived sources to CD8(+) cytotoxic T lymphocytes (CTL), with recognition of a foreign peptide normally targeting the cell for lysis. It is generally thought that the high level of MHC polymorphism, which is concentrated mostly within the peptide-binding groove, is driven by the 'evolutionary arms race' against pathogens. Many pathogens have developed novel and intriguing mechanisms for evading the continuous sampling of the intracellular and intercellular environments by MHC molecules, none more so than viruses. The characterization of immunoevasion mechanisms has improved our understanding of MHC biology. This review will highlight our current understanding of the MHC class I biosynthetic pathway and how it has been exploited by pathogens, especially viruses, to potentially evade CTL recognition.
主要组织相容性复合体（MHC）I类分子结合并呈递来自内源性或外源性来源的短抗原肽给CD8(+)细胞毒性T淋巴细胞（CTL），识别外来肽通常会靶向细胞进行裂解。一般认为，高度的MHC多态性主要集中在肽结合槽内，是由与病原体的“进化军备竞赛”驱动的。许多病原体已经开发出新颖且引人入胜的机制来逃避MHC分子对细胞内和细胞间环境的持续监测，其中病毒尤为突出。免疫逃避机制的特征增进了我们对MHC生物学的理解。本综述将重点介绍我们目前对MHC I类生物合成途径的理解，以及病原体，特别是病毒如何利用该途径来潜在地逃避CTL识别。
