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首页> 外文期刊>Trends in immunology >Neutrophil beta2 integrins: moderators of life or death decisions.
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Neutrophil beta2 integrins: moderators of life or death decisions.

机译：中性粒细胞beta2整合素：生命或死亡决定的调节者。

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摘要

Beta2 integrins are leukocyte-specific membrane receptors that are crucial for host defense. They are best known for promoting neutrophil recruitment into inflamed tissue and pathogen phagocytosis. More recent data suggest that they also modulate neutrophil apoptosis. Neutrophils are terminally differentiated cells, which undergo constitutive apoptosis, and their apoptosis and clearance is required for the resolution of inflammation. Engagement of the beta2 integrin Mac-1 through its adhesion to its ligands, intercellular adhesion molecule-1 (ICAM-1) and fibrinogen, signals survival cues in neutrophils. However, in the presence of pro-apoptotic signals, such as tumor necrosis factor (TNF), Mac-1 engagement accelerates apoptosis. Furthermore, Mac-1-dependent phagocytosis of complement-opsonized pathogens triggers rapid neutrophil apoptosis, which is dependent on NADPH oxidase-generated reactive oxygen species and caspase activation. This is also associated with changes in the transcription profiles of pro- and anti-apoptotic genes. In this review, the beta2 integrin-dependent mechanisms that modulate the decision between life and death in neutrophils are overviewed.
机译：Beta2整合素是白细胞特异性膜受体，对宿主防御至关重要。它们以促进中性粒细胞募集进入发炎组织和病原体吞噬作用而闻名。最近的数据表明它们还调节中性粒细胞凋亡。中性粒细胞是终末分化的细胞，其经历组成性凋亡，其凋亡和清除对于解决炎症是必需的。 β2整合素Mac-1通过其与配体，细胞间粘附分子1（ICAM-1）和纤维蛋白原的粘附而参与其中，标志着嗜中性粒细胞的存活线索。但是，在存在促凋亡信号（例如肿瘤坏死因子（TNF））的情况下，Mac-1参与加速了细胞凋亡。此外，补体调理病原体的Mac-1依赖性吞噬作用会触发中性粒细胞快速凋亡，这依赖于NADPH氧化酶生成的活性氧和半胱天冬酶的活化。这也与促凋亡和抗凋亡基因的转录谱的变化有关。在这篇综述中，概述了β2整合素依赖性机制，可调节嗜中性粒细胞的生与死之间的决定。

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