Yokoyama W M, Seaman W E
Department of Medicine, Mount Sinai School of Medicine, New York City, New York 10029-6574.
Annu Rev Immunol. 1993;11:613-35. doi: 10.1146/annurev.iy.11.040193.003145.
Natural killer cells lyse tumor and virally infected cells in a specific manner that has not been molecularly characterized. Target cell expression of major histocompatibility complex (MHC) class I molecules is correlated with target cell resistance to natural killing. A mechanism to explain this observation is that NK cells may display two types of recognition and activation molecules that have opposing functions when bound to target cell ligands. One type of surface receptor such as the NKR-P1 molecule may activate NK activity whereas the other, represented by the mouse Ly-49 molecule, may engage target cell MHC molecules and inhibit cytotoxicity by transducing "negative" signals. NKR-P1 and Ly-49 are structurally related, and they are encoded by genetically linked loci in a chromosomal region, termed the NK gene complex (NKC), on distal mouse chromosome 6. Target cell susceptibility to natural killing may be dependent upon specific ligand-receptor interaction with these activating or inhibitory NKC-encoded molecules.
自然杀伤细胞以一种尚未在分子水平上得到表征的特定方式裂解肿瘤细胞和病毒感染细胞。主要组织相容性复合体(MHC)I类分子在靶细胞上的表达与靶细胞对自然杀伤的抗性相关。解释这一观察结果的一种机制是,自然杀伤细胞可能展示两种类型的识别和激活分子,当它们与靶细胞配体结合时具有相反的功能。一种表面受体,如NKR-P1分子,可能激活自然杀伤活性,而另一种以小鼠Ly-49分子为代表,可能与靶细胞MHC分子结合,并通过转导“负”信号来抑制细胞毒性。NKR-P1和Ly-49在结构上相关,它们由位于小鼠6号染色体远端一个称为自然杀伤基因复合体(NKC)的染色体区域中基因连锁的位点编码。靶细胞对自然杀伤的易感性可能取决于与这些由NKC编码的激活或抑制分子的特异性配体-受体相互作用。