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通过非经典主要组织相容性复合体和非主要组织相容性复合体配体进行自然杀伤细胞教育

NK cell education via nonclassical MHC and non-MHC ligands.

作者信息

He Yuke, Tian Zhigang

机构信息

Institute of Immunology, Key Laboratory of Innate Immunity and Chronic Disease of Chinese Academy of Science, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei 230027, China.

Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, China.

出版信息

Cell Mol Immunol. 2017 Apr;14(4):321-330. doi: 10.1038/cmi.2016.26. Epub 2016 Jun 6.

DOI:10.1038/cmi.2016.26
PMID:27264685
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5380944/
Abstract

Natural killer (NK) cell education, a process for achieving functional maturation and self-tolerance, has been previously defined by the interaction between self-major histocompatibility complex class I (MHC-I) molecules and their specific inhibitory receptors. Over the past several years, growing evidence has highlighted the important roles of nonclassical MHC-I and non-MHC-I molecules in NK cell education. Herein, we review the current knowledge of NK cell education, with a particular focus on nonclassical MHC-I- and non-MHC-I-dependent education, and compare them with the classical MHC-I-dependent education theory. In addition, we update and extend this theory by presenting the 'Confining Model', discussing cis and trans characteristics, reassessing quantity and quality control, and elucidating the redundancy of NK cell education in tumor and virus infection.

摘要

自然杀伤(NK)细胞驯化是实现功能成熟和自我耐受的过程,此前已通过自身主要组织相容性复合体I类(MHC-I)分子与其特定抑制性受体之间的相互作用来定义。在过去几年中,越来越多的证据凸显了非经典MHC-I分子和非MHC-I分子在NK细胞驯化中的重要作用。在此,我们综述了目前关于NK细胞驯化的知识,特别关注非经典MHC-I依赖性和非MHC-I依赖性驯化,并将它们与经典MHC-I依赖性驯化理论进行比较。此外,我们通过提出“限制模型”、讨论顺式和反式特征、重新评估数量和质量控制以及阐明肿瘤和病毒感染中NK细胞驯化的冗余性来更新和扩展这一理论。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0394/5380944/58743c16c74b/cmi201626f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0394/5380944/debfba0a0a77/cmi201626f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0394/5380944/35d4fac78604/cmi201626f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0394/5380944/58743c16c74b/cmi201626f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0394/5380944/debfba0a0a77/cmi201626f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0394/5380944/35d4fac78604/cmi201626f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0394/5380944/58743c16c74b/cmi201626f3.jpg

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Nat Immunol. 2016 Apr;17(4):387-96. doi: 10.1038/ni.3369. Epub 2016 Feb 15.
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