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血小板:中性粒细胞胞外陷阱形成中的新“砖块”

Platelets: New Bricks in the Building of Neutrophil Extracellular Traps.

作者信息

Carestia Agostina, Kaufman Tomas, Schattner Mirta

机构信息

Laboratory of Experimental Thrombosis, Institute of Experimental Medicine-CONICET, National Academy of Medicine , Buenos Aires , Argentina.

出版信息

Front Immunol. 2016 Jul 6;7:271. doi: 10.3389/fimmu.2016.00271. eCollection 2016.

DOI:10.3389/fimmu.2016.00271
PMID:27458459
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4933697/
Abstract

In addition to being key elements in hemostasis and thrombosis, platelets have an important role in the inflammatory and innate immune response. This activity is associated with their capability to recognize pathogens through the expression of toll-like receptors, the secretion of various cytokines, chemokines, and growth factors stored within their granules, and the expression of cell adhesion molecules that allows interaction with other immune cells, mainly neutrophils and monocytes. As part of the first line of defense, neutrophils control invading pathogens by phagocytosis, the release of antimicrobial proteins during degranulation, or through the formation of web-like structures named neutrophil extracellular traps (NETs). NETs are formed by chromatin, proteases, and antimicrobial proteins, and their main function is to trap and kill bacteria, virus, and fungi, avoiding their dissemination. Besides microorganisms, NET formation is also triggered by proinflammatory molecules and platelets. The uncontrolled formation of NETs might exert tissue damage and has been involved in a pathogenic mechanism of autoimmune and prothrombotic clinical conditions. In this review, we discuss the role of platelets in NET generation highlighting the mediators, stimuli, and molecular mechanisms involved in this phenomenon, both in human and murine models.

摘要

除了作为止血和血栓形成的关键要素外,血小板在炎症和固有免疫反应中也发挥着重要作用。这种活性与其通过Toll样受体的表达识别病原体、分泌储存在其颗粒内的各种细胞因子、趋化因子和生长因子以及表达允许与其他免疫细胞(主要是中性粒细胞和单核细胞)相互作用的细胞粘附分子的能力相关。作为第一道防线的一部分,中性粒细胞通过吞噬作用、脱颗粒过程中抗菌蛋白的释放或通过形成称为中性粒细胞胞外陷阱(NETs)的网状结构来控制入侵的病原体。NETs由染色质、蛋白酶和抗菌蛋白组成,其主要功能是捕获和杀死细菌、病毒和真菌,防止它们扩散。除了微生物外,NET的形成也由促炎分子和血小板触发。NET的不受控制形成可能会造成组织损伤,并参与自身免疫和血栓形成临床病症的致病机制。在这篇综述中,我们讨论血小板在NET生成中的作用,重点介绍在人类和小鼠模型中参与这一现象的介质、刺激因素和分子机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4817/4933697/ea6bc34e0ab0/fimmu-07-00271-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4817/4933697/b4e53d58f3cd/fimmu-07-00271-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4817/4933697/ea6bc34e0ab0/fimmu-07-00271-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4817/4933697/b4e53d58f3cd/fimmu-07-00271-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4817/4933697/ea6bc34e0ab0/fimmu-07-00271-g002.jpg

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Neutrophil elastase-deficient mice form neutrophil extracellular traps in an experimental model of deep vein thrombosis.
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