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自身配体调节激活自然杀伤细胞受体。

Regulation of self-ligands for activating natural killer cell receptors.

机构信息

Immunology Programme, Centre for Life Sciences, Department of Microbiology, National University of Singapore 117456, Singapore.

出版信息

Ann Med. 2013 Jun;45(4):384-94. doi: 10.3109/07853890.2013.792495. Epub 2013 May 23.

DOI:10.3109/07853890.2013.792495
PMID:23701136
Abstract

Natural killer (NK) cells are able to lyse infected and tumor cells while sparing healthy cells. Recognition of diseased cells by NK cells is governed by several activating and inhibitory receptors. We review numerous pathways that have been implicated in the regulation of self-ligands for activating receptors, including NKG2D, DNAM-1, LFA-1, NKp30, NKp44, NKp46, NKp65, and NKp80 found on NK cells and some T cells. Understanding how the regulation of self-encoded ligand expression is regulated may provide novel avenues for future therapeutic approaches to infections and cancer.

摘要

自然杀伤 (NK) 细胞能够裂解感染和肿瘤细胞,而对健康细胞则具有耐受性。NK 细胞对病变细胞的识别受几种激活和抑制受体的控制。我们综述了许多与调节激活受体自身配体有关的途径,包括 NK 细胞和某些 T 细胞上的 NKG2D、DNAM-1、LFA-1、NKp30、NKp44、NKp46、NKp65 和 NKp80。了解自我编码配体表达的调控如何被调节,可能为感染和癌症的未来治疗方法提供新的途径。

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