Regulation of ligands for the NKG2D activating receptor.

Regulation of ligands for the NKG2D activating receptor.
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DOI:
10.1146/annurev-immunol-032712-095951
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发表时间:
2013
影响因子:
29.7
通讯作者:
Jung H
Jung H
中科院分区:
医学1区
文献类型:
--
作者:
Raulet DH;Gasser S;Gowen BG;Deng W;Jung H

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NKG2D 是所有 NK 细胞和 T 细胞亚群表达的激活受体。它作为检测和消除转化和感染细胞的主要识别受体,并参与多种炎症性疾病的发生。 NKG2D 的配体是由在某些病理生理状态下活跃的途径诱导的自身蛋白。 NKG2D 配体在 mRNA 和蛋白质稳定性水平以及通过细胞表面裂解进行转录调节。在某些情况下,配体诱导可归因于在癌细胞或感染细胞中特异性激活的途径。我们回顾了与 NKG2D 配体调节有关的众多途径,讨论了这些途径可能发挥作用的病理状态,并尝试将这些发现综合成 NKG2D 配体调节 NK 细胞对癌症和感染反应的一般方案。
NKG2D is an activating receptor expressed by all NK cells and subsets of T cells. It serves as a major recognition receptor for detection and elimination of transformed and infected cells and participates in the genesis of several inflammatory diseases. The ligands for NKG2D are self-proteins that are induced by pathways that are active in certain pathophysiological states. NKG2D ligands are regulated transcriptionally, at the level of mRNA and protein stability, and by cleavage from the cell surface. In some cases, ligand induction can be attributed to pathways that are activated specifically in cancer cells or infected cells. We review the numerous pathways that have been implicated in the regulation of NKG2D ligands, discuss the pathologic states in which those pathways are likely to act, and attempt to synthesize the findings into general schemes of NKG2D ligand regulation in NK cell responses to cancer and infection.
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