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白细胞向炎症组织的迁移。

Leukocyte migration into inflamed tissues.

机构信息

William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.

Department of Immunology, Weizmann Institute of Science, Rehovot 76100 Israel.

出版信息

Immunity. 2014 Nov 20;41(5):694-707. doi: 10.1016/j.immuni.2014.10.008.

DOI:10.1016/j.immuni.2014.10.008
PMID:25517612
Abstract

Leukocyte migration through activated venular walls is a fundamental immune response that is prerequisite to the entry of effector cells such as neutrophils, monocytes, and effector T cells to sites of infection, injury, and stress within the interstitium. Stimulation of leukocytes is instrumental in this process with enhanced temporally controlled leukocyte adhesiveness and shape-changes promoting leukocyte attachment to the inner wall of blood vessels under hydrodynamic forces. This initiates polarized motility of leukocytes within and through venular walls and transient barrier disruption facilitated sequentially by stimulated vascular cells, i.e., endothelial cells and their associated pericytes. Perivascular cells such as macrophages and mast cells that act as tissue inflammatory sentinels can also directly and indirectly regulate the exit of leukocytes from the vascular lumen. In this review, we discuss current knowledge and open questions regarding the mechanisms involved in the interactions of different effector leukocytes with peripheral vessels in extralymphoid organs.

摘要

白细胞穿过活化的小静脉壁的迁移是一种基本的免疫反应,是效应细胞(如中性粒细胞、单核细胞和效应 T 细胞)进入间质中感染、损伤和应激部位的先决条件。白细胞的刺激在这个过程中起着重要作用,增强了时间控制的白细胞黏附性和形态变化,促进了白细胞在水力作用下附着在血管内壁上。这启动了白细胞在小静脉壁内和穿过小静脉壁的极化运动,并通过受刺激的血管细胞(即内皮细胞及其相关周细胞)依次促进短暂的屏障破坏。作为组织炎症哨兵的血管周细胞,如巨噬细胞和肥大细胞,也可以直接和间接地调节白细胞从小血管腔中的逸出。在这篇综述中,我们讨论了关于不同效应白细胞与淋巴器官外周围血管相互作用的机制的现有知识和悬而未决的问题。

相似文献

1
Leukocyte migration into inflamed tissues.白细胞向炎症组织的迁移。
Immunity. 2014 Nov 20;41(5):694-707. doi: 10.1016/j.immuni.2014.10.008.
2
Endothelial actin-binding proteins and actin dynamics in leukocyte transendothelial migration.白细胞跨内皮迁移中的内皮肌动蛋白结合蛋白与肌动蛋白动力学
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Transendothelial migration of effector T cells across inflamed endothelial barriers does not require heparan sulfate proteoglycans.效应T细胞穿过炎症性内皮屏障的跨内皮迁移不需要硫酸乙酰肝素蛋白聚糖。
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Endothelial junction regulation: a prerequisite for leukocytes crossing the vessel wall.内皮细胞连接调控:白细胞穿越血管壁的必要前提。
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The junctional adhesion molecule JAM-C regulates polarized transendothelial migration of neutrophils in vivo.连接黏附分子 JAM-C 调控体内中性粒细胞的极化跨内皮迁移。
Nat Immunol. 2011 Jun 26;12(8):761-9. doi: 10.1038/ni.2062.
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Mechanisms of leukocyte transendothelial migration.白细胞跨内皮迁移的机制。
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Recombinant lectin-like domain of thrombomodulin suppresses vascular inflammation by reducing leukocyte recruitment via interacting with Lewis Y on endothelial cells.血栓调节蛋白的重组凝集素样结构域通过与内皮细胞上的 Lewis Y 相互作用减少白细胞募集来抑制血管炎症。
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Relevance of endothelial junctions in leukocyte extravasation and vascular permeability.内皮细胞连接在白细胞渗出和血管通透性中的相关性。
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Basic fibroblast growth factor (bFGF, FGF-2) potentiates leukocyte recruitment to inflammation by enhancing endothelial adhesion molecule expression.碱性成纤维细胞生长因子(bFGF,FGF - 2)通过增强内皮细胞黏附分子的表达,增强白细胞向炎症部位的募集。
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Consequences of leukocyte-vessel wall interactions in inflammatory and immune reactions.炎症和免疫反应中白细胞与血管壁相互作用的后果。
Semin Thromb Hemost. 1987 Oct;13(4):434-44. doi: 10.1055/s-2007-1003520.

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