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激活型自然杀伤细胞受体的参与及其在病原体免疫中的调节作用。

Involvement of activating NK cell receptors and their modulation in pathogen immunity.

作者信息

Marras Francesco, Bozzano Federica, De Maria Andrea

机构信息

Centro di Eccellenza per la Ricerca Biomedica (CEBR), Università di Genova, Genova, Italy.

出版信息

J Biomed Biotechnol. 2011;2011:152430. doi: 10.1155/2011/152430. Epub 2011 Aug 11.

DOI:10.1155/2011/152430
PMID:21860586
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3155793/
Abstract

Natural Killer (NK) cells are endowed with cell-structure-sensing receptors providing inhibitory protection from self-destruction (inhibitory NK receptors, iNKRs, including killer inhibitory receptors and other molecules) and rapid triggering potential leading to functional cell activation by Toll-like receptors (TLRs), cytokine receptors, and activating NK cell receptors including natural cytotoxicity receptors (NCRs, i.e., NKp46, NKp46, and NKp44). NCR and NKG2D recognize ligands on infected cells which may be endogenous or may directly bind to some structures derived from invading pathogens. In this paper, we address the known direct or indirect interactions between activating receptors and pathogens and their expression during chronic HIV and HCV infections.

摘要

自然杀伤(NK)细胞具有细胞结构传感受体,这些受体提供抑制性保护以防止自身破坏(抑制性NK受体,iNKRs,包括杀伤细胞抑制受体和其他分子),以及通过Toll样受体(TLRs)、细胞因子受体和包括自然细胞毒性受体(NCRs,即NKp46、NKp46和NKp44)在内的激活NK细胞受体导致功能性细胞激活的快速触发潜能。NCR和NKG2D识别感染细胞上的配体,这些配体可能是内源性的,也可能直接结合某些源自入侵病原体的结构。在本文中,我们探讨了激活受体与病原体之间已知的直接或间接相互作用及其在慢性HIV和HCV感染期间的表达。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7de/3155793/b0e09e6ff19d/JBB2011-152430.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7de/3155793/4c4f6ccc401c/JBB2011-152430.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7de/3155793/b0e09e6ff19d/JBB2011-152430.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7de/3155793/4c4f6ccc401c/JBB2011-152430.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7de/3155793/b0e09e6ff19d/JBB2011-152430.002.jpg

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Eur J Immunol. 2011 Oct;41(10):2905-14. doi: 10.1002/eji.201041361.
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NK-cell phenotype at interruption underlies widely divergent duration of CD4+-guided antiretroviral treatment interruption.NK 细胞表型在中断时的表现,是导致 CD4+指导的抗逆转录病毒治疗中断时间差异的主要原因。
Int Immunol. 2011 Feb;23(2):109-18. doi: 10.1093/intimm/dxq462. Epub 2011 Jan 7.
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腺苷信号转导改变自然杀伤细胞的功能反应。
Front Immunol. 2018 Oct 30;9:2533. doi: 10.3389/fimmu.2018.02533. eCollection 2018.
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Immunology. 2018 Dec;155(4):467-476. doi: 10.1111/imm.12986. Epub 2018 Aug 14.
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