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趋化因子对中性粒细胞呼吸爆发的激活作用:质膜中N-甲酰肽受体的调节

Activation of the neutrophil respiratory burst by chemoattractants: regulation of the N-formyl peptide receptor in the plasma membrane.

作者信息

Jesaitis A J, Allen R A

机构信息

Department of Immunology, Scripps Clinic and Research Foundation, La Jolla, California 92037.

出版信息

J Bioenerg Biomembr. 1988 Dec;20(6):679-707. doi: 10.1007/BF00762548.

DOI:10.1007/BF00762548
PMID:2854128
Abstract

The N-formyl peptide receptor mediates a number of host defensive responses of human neutrophils that result in chemotaxis, secretion of hydrolytic enzymes, and superoxide generation. Inappropriate activation or defective regulation of these responses can result in pathogenic states responsible for inflammatory disease. The receptor is a 50 to 70-kD, integral plasma membrane glycoprotein with intracellular and surface localization. Its abundance in the membrane is regulated by membrane flow and recycling processes. Cytoskeletal interactions are believed to control its organization in the plane of the membrane and interaction with other proteins. The receptor's most important interaction is with guanyl nucleotide binding proteins that serve as signal transduction partners ultimately leading to activation of effector responses. Because the interaction of the receptor with G proteins is necessary for transduction, control of this interaction may be at the root of understanding the molecular control of responses in these cells. This review briefly summarizes some of the molecular properties, dynamics, and interactions of this receptor system in human neutrophils and discusses how these characteristics may pertain to the activation and control of superoxide generation.

摘要

N-甲酰基肽受体介导人类中性粒细胞的多种宿主防御反应,这些反应会导致趋化作用、水解酶分泌和超氧化物生成。这些反应的不适当激活或调节缺陷可导致引发炎症性疾病的致病状态。该受体是一种50至70kD的整合质膜糖蛋白,具有细胞内和表面定位。其在膜中的丰度受膜流动和循环过程调节。细胞骨架相互作用被认为控制其在膜平面内的组织以及与其他蛋白质的相互作用。该受体最重要的相互作用是与鸟苷酸结合蛋白,这些蛋白作为信号转导伙伴最终导致效应反应的激活。由于受体与G蛋白的相互作用对于转导是必需的,因此对这种相互作用的控制可能是理解这些细胞中反应分子控制的根源。本综述简要总结了该受体系统在人类中性粒细胞中的一些分子特性及动力学和相互作用,并讨论了这些特性如何与超氧化物生成的激活和控制相关。

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