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血小板与固有免疫。

Platelets and innate immunity.

机构信息

Keenan Research Centre, Li Ka Shing Knowledge Institute, St. Michael's Hospital, 30 Bond Street, Toronto, ON M5B 1W8, Canada.

出版信息

Cell Mol Life Sci. 2010 Feb;67(4):499-511. doi: 10.1007/s00018-009-0205-1. Epub 2009 Dec 18.

DOI:10.1007/s00018-009-0205-1
PMID:20016997
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11115613/
Abstract

Although platelets are best known as primary mediators of hemostasis, this function intimately associates them with inflammatory processes, and it has been increasingly recognized that platelets play an active role in both innate and adaptive immunity. For example, platelet adhesive interactions with leukocytes and endothelial cells via P-selectin can lead to several pro-inflammatory events, including leukocyte rolling and activation, production of cytokine cascades, and recruitment of the leukocytes to sites of tissue damage. Superimposed on this, platelets express immunologically-related molecules such as CD40L and Toll-like receptors that have been shown to functionally modulate innate immunity. Furthermore, platelets themselves can interact with microorganisms, and several viruses have been shown to cross-react immunologically with platelet antigens. This review discusses the central role that platelets play in inflammation, linking them with varied pathological conditions, such as atherosclerosis, sepsis, and immune thrombocytopenic purpura, and suggests that platelets also act as primary mediators of our innate defences.

摘要

虽然血小板作为止血的主要介质而广为人知,但这一功能使它们与炎症过程密切相关,并且人们越来越认识到血小板在先天免疫和适应性免疫中都发挥着积极作用。例如,血小板通过 P 选择素与白细胞和内皮细胞的黏附相互作用可导致多种促炎事件,包括白细胞滚动和激活、细胞因子级联的产生以及白细胞向组织损伤部位的募集。在此基础上,血小板表达免疫相关分子,如 CD40L 和 Toll 样受体,这些分子已被证明可调节先天免疫。此外,血小板本身可以与微生物相互作用,一些病毒已被证明在免疫学上与血小板抗原发生交叉反应。这篇综述讨论了血小板在炎症中的核心作用,将其与动脉粥样硬化、败血症和免疫性血小板减少性紫癜等多种病理状况联系起来,并表明血小板也作为我们先天防御的主要介质发挥作用。

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本文引用的文献

1
A Decapod Hemocyte Classification Scheme Integrating Morphology, Cytochemistry, and Function.一种整合形态学、细胞化学和功能的十足目血细胞分类方案。
Biol Bull. 1990 Feb;178(1):33-45. doi: 10.2307/1541535.
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Lipopolysaccharide stimulates platelet secretion and potentiates platelet aggregation via TLR4/MyD88 and the cGMP-dependent protein kinase pathway.脂多糖通过Toll样受体4/髓样分化因子88(TLR4/MyD88)和环磷酸鸟苷(cGMP)依赖性蛋白激酶途径刺激血小板分泌并增强血小板聚集。
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[Platelets "Toll-like receptor" engagement stimulates the release of immunomodulating molecules].血小板“Toll样受体”的激活刺激免疫调节分子的释放
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A novel immunosuppressive pathway involving peroxynitrite-mediated [corrected] nitration of platelet antigens within antigen-presenting cells.一种涉及过氧亚硝酸盐介导的抗原呈递细胞内血小板抗原硝化作用的新型免疫抑制途径。 (注:原文中“[corrected]”可能是编辑说明之类的内容,这里按字面保留并翻译,整体不影响主要意思理解)
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Estrogen, inflammation, and platelet phenotype.雌激素、炎症与血小板表型。
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Platelet activation by Histophilus somni and its lipooligosaccharide induces endothelial cell proinflammatory responses and platelet internalization.睡眠嗜血杆菌及其脂寡糖激活血小板可诱导内皮细胞产生促炎反应和血小板内化。
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Transfusion-related acute lung injury.输血相关急性肺损伤
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Platelet-vessel wall interactions in atherosclerotic disease.动脉粥样硬化疾病中的血小板-血管壁相互作用。
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Toll-like receptor 4 ligand can differentially modulate the release of cytokines by human platelets.Toll样受体4配体可不同程度地调节人血小板细胞因子的释放。
Br J Haematol. 2008 Apr;141(1):84-91. doi: 10.1111/j.1365-2141.2008.06999.x. Epub 2008 Feb 12.