Reprint of Neutrophil cell surface receptors and their intracellular signal transduction pathways

被引:163
作者
Futosi, Krisztina [1 ]
Fodor, Szabina [2 ]
Mocsai, Attila [1 ]
机构
[1] Semmelweis Univ, Sch Med, Dept Physiol, H-1094 Budapest, Hungary
[2] Corvinus Univ Budapest, Dept Comp Sci, H-1093 Budapest, Hungary
基金
英国惠康基金; 欧洲研究理事会;
关键词
Neutrophils; Signaling; Receptors; Kinases; Inflammation; SRC-FAMILY KINASES; LEUKOCYTE ADHESION DEFICIENCY; COLONY-STIMULATING FACTOR; ACTIVATED PROTEIN-KINASE; NF-KAPPA-B; HIGH-AFFINITY RECEPTOR; BETA-GAMMA-SUBUNIT; FORMYL PEPTIDE RECEPTORS; TOLL-LIKE RECEPTORS; NOD-LIKE RECEPTORS;
D O I
10.1016/j.intimp.2013.11.010
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Neutrophils play a critical role in the host defense against bacterial and fungal infections, but their inappropriate activation also contributes to tissue damage during autoimmune and inflammatory diseases. Neutrophils express a large number of cell surface receptors for the recognition of pathogen invasion and the inflammatory environment Those include G-protein-coupled chemokine and chemoattractant receptors, Pc-receptors, adhesion receptors such as selectins/selectin ligands and integrins, various cytokine receptors, as well as innate immune receptors such as Toll-like receptors and C-type lectins. The various cell surface receptors trigger very diverse signal transduction pathways including activation of heterotrimeric and monomeric G-proteins, receptor-induced and store-operated Ca2+ signals, protein and lipid kinases, adapter proteins and cytoskeletal rearrangement. Here we provide an overview of the receptors involved in neutrophil activation and the intracellular signal transduction processes they trigger. This knowledge is crucial for understanding how neutrophils participate in antimicrobial host defense and inflammatory tissue damage and may also point to possible future targets of the pharmacological therapy of neutrophil-mediated autoimmune or inflammatory diseases. (C) 2013 The Authors. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:1185 / 1197
页数:13
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