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本文引用的文献

1
Neutrophils scan for activated platelets to initiate inflammation.中性粒细胞扫描激活的血小板以启动炎症反应。
Science. 2014 Dec 5;346(6214):1234-8. doi: 10.1126/science.1256478. Epub 2014 Dec 4.
2
Investigational selectin-targeted therapy of sickle cell disease.镰状细胞病的研究性选择素靶向治疗
Expert Opin Investig Drugs. 2015 Feb;24(2):229-38. doi: 10.1517/13543784.2015.963552. Epub 2014 Sep 22.
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The Src family kinases Hck, Fgr, and Lyn are critical for the generation of the in vivo inflammatory environment without a direct role in leukocyte recruitment.Src家族激酶Hck、Fgr和Lyn对于体内炎症环境的产生至关重要,而在白细胞募集中没有直接作用。
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Src family kinases: at the forefront of platelet activation.Src家族激酶:血小板活化的前沿
Blood. 2014 Sep 25;124(13):2013-24. doi: 10.1182/blood-2014-01-453134. Epub 2014 Aug 12.
5
Immobilized immune complexes induce neutrophil extracellular trap release by human neutrophil granulocytes via FcγRIIIB and Mac-1.固定化免疫复合物通过 FcγRIIIB 和 Mac-1 诱导人中性粒细胞释放中性粒细胞胞外诱捕网。
J Immunol. 2014 Aug 15;193(4):1954-65. doi: 10.4049/jimmunol.1400478. Epub 2014 Jul 14.
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The role and regulation of complement activation as part of the thromboinflammation elicited in cell therapies.补体激活作为细胞治疗中引发血栓炎症的一部分的作用和调节。
Mol Immunol. 2014 Oct;61(2):185-90. doi: 10.1016/j.molimm.2014.06.009. Epub 2014 Jul 3.
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Factor XII: a drug target for safe interference with thrombosis and inflammation.凝血因子 XII:安全干预血栓形成和炎症的药物靶点。
Drug Discov Today. 2014 Sep;19(9):1459-64. doi: 10.1016/j.drudis.2014.06.024. Epub 2014 Jun 30.
8
Phase 1 study of the E-selectin inhibitor GMI 1070 in patients with sickle cell anemia.E-选择素抑制剂GMI 1070用于镰状细胞贫血患者的1期研究。
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9
Phosphodiesterase type 4 blockade prevents platelet-mediated neutrophil recruitment at the site of vascular injury.4型磷酸二酯酶阻断可防止血小板介导的中性粒细胞在血管损伤部位募集。
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10
microRNA expression in peripheral blood cells following acute ischemic stroke and their predicted gene targets.急性缺血性中风后外周血细胞中的微小RNA表达及其预测的基因靶点。
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血栓炎症条件下的血小板-中性粒细胞相互作用

Platelet-neutrophil interactions under thromboinflammatory conditions.

作者信息

Li Jing, Kim Kyungho, Barazia Andrew, Tseng Alan, Cho Jaehyung

机构信息

Department of Pharmacology, University of Illinois College of Medicine, 835 S. Wolcott Ave, E403, Chicago, IL, 60612, USA.

出版信息

Cell Mol Life Sci. 2015 Jul;72(14):2627-43. doi: 10.1007/s00018-015-1845-y. Epub 2015 Feb 4.

DOI:10.1007/s00018-015-1845-y
PMID:25650236
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4480154/
Abstract

Platelets primarily mediate hemostasis and thrombosis, whereas leukocytes are responsible for immune responses. Since platelets interact with leukocytes at the site of vascular injury, thrombosis and vascular inflammation are closely intertwined and occur consecutively. Recent studies using real-time imaging technology demonstrated that platelet-neutrophil interactions on the activated endothelium are an important determinant of microvascular occlusion during thromboinflammatory disease in which inflammation is coupled to thrombosis. Although the major receptors and counter receptors have been identified, it remains poorly understood how heterotypic platelet-neutrophil interactions are regulated under disease conditions. This review discusses our current understanding of the regulatory mechanisms of platelet-neutrophil interactions in thromboinflammatory disease.

摘要

血小板主要介导止血和血栓形成,而白细胞负责免疫反应。由于血小板在血管损伤部位与白细胞相互作用,血栓形成和血管炎症紧密相连且相继发生。最近使用实时成像技术的研究表明,在炎症与血栓形成相关联的血栓炎症性疾病中,活化内皮细胞上的血小板 - 中性粒细胞相互作用是微血管阻塞的重要决定因素。尽管主要的受体和反受体已被确定,但在疾病状态下异型血小板 - 中性粒细胞相互作用是如何被调节的仍知之甚少。本综述讨论了我们目前对血栓炎症性疾病中血小板 - 中性粒细胞相互作用调节机制的理解。