Extending missing-self? Functional interactions between lectin-like NKrp1 receptors on NK cells with lectin-like ligands.

Extending missing-self? Functional interactions between lectin-like NKrp1 receptors on NK cells with lectin-like ligands.
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DOI:
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发表时间:
2006
影响因子:
--
通讯作者:
W. M. Yokoyama
W. M. Yokoyama
中科院分区:
医学3区
文献类型:
--
作者:
B. F. M. Plougastel;W. M. Yokoyama

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自然杀伤(NK)细胞的功能明显受到主要组织相容性复合体(MHC)I类分子对其细胞靶点的调节。在小鼠中,这是由于属于Ly 49家族的MHC特异性抑制性受体的作用。Ly 49受体在NK基因复合物(NKC)中编码,所述NK基因复合物含有NK细胞和其他造血细胞上的其他凝集素样受体的基因簇。有趣的是,最近的研究表明,这些凝集素样受体中的一些,属于Nkrpl家族,可以识别其他凝集素样分子,称为Clr,也编码在NKC中。这些受体-配体对的遗传连锁位点表明了一种遗传策略,以保持这种相互作用,并显示了与Ly 49-MHC相互作用的其他几个对比。在这篇综述中,我们讨论了这些问题,并总结了最近的事态发展,这种非MHC依赖性调节NK细胞功能。
The functions of natural killer (NK) cells are clearly regulated by major histocompatibility complex (MHC) class I molecules on their cellular targets. In mice, this is due to the action of MHC-specific inhibitory receptors belonging to the Ly49 family oflectin-like molecules. The Ly49 receptors are encoded in the NK gene complex (NKC) that contains clusters of genes for other lectin-like receptors on NK cells and other hematopoietic cells. Interestingly, recent studies have shown that some of these lectin-like receptors, belonging to the Nkrpl family, can recognize other lectin-like molecules, termed Clr, also encoded in the NKC. These genetically linked loci for receptor-ligand pairs suggest a genetic strategy to preserve this interaction and show several other contrasts with Ly49-MHC interactions. In this review, we discuss these issues and summarize recent developments concerning this non-MHC-dependent regulation of NK cell function.
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