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吞噬作用之外的额外呼吸:NADPH 氧化酶 2 在适应性免疫和炎症中的作用。

Beyond the Extra Respiration of Phagocytosis: NADPH Oxidase 2 in Adaptive Immunity and Inflammation.

机构信息

Centre for Inflammatory Disease, Department of Immunology & Inflammation, Imperial College, London, United Kingdom.

出版信息

Front Immunol. 2021 Sep 1;12:733918. doi: 10.3389/fimmu.2021.733918. eCollection 2021.

DOI:10.3389/fimmu.2021.733918
PMID:34539670
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8440999/
Abstract

Reactive oxygen species (ROS) derived from the phagocyte NADPH oxidase (NOX2) are essential for host defence and immunoregulation. Their levels must be tightly controlled. ROS are required to prevent infection and are used in signalling to regulate several processes that are essential for normal immunity. A lack of ROS then leads to immunodeficiency and autoinflammation. However, excess ROS are also deleterious, damaging tissues by causing oxidative stress. In this review, we focus on two particular aspects of ROS biology: (i) the emerging understanding that NOX2-derived ROS play a pivotal role in the development and maintenance of adaptive immunity and (ii) the effects of excess ROS in systemic disease and how limiting ROS might represent a therapeutic avenue in limiting excess inflammation.

摘要

活性氧(ROS)来源于吞噬细胞 NADPH 氧化酶(NOX2),对宿主防御和免疫调节至关重要。它们的水平必须严格控制。ROS 用于预防感染,并用于信号转导以调节几种对正常免疫至关重要的过程。缺乏 ROS 会导致免疫缺陷和自身炎症。然而,过多的 ROS 也是有害的,通过引起氧化应激来破坏组织。在这篇综述中,我们重点关注 ROS 生物学的两个特定方面:(i)越来越多的人认为,NOX2 衍生的 ROS 在适应性免疫的发展和维持中起着关键作用;(ii)过量 ROS 在系统性疾病中的作用,以及限制 ROS 可能成为限制过度炎症的治疗途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d877/8440999/301e39dca485/fimmu-12-733918-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d877/8440999/0e1d318ef0ea/fimmu-12-733918-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d877/8440999/301e39dca485/fimmu-12-733918-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d877/8440999/0e1d318ef0ea/fimmu-12-733918-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d877/8440999/301e39dca485/fimmu-12-733918-g002.jpg

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