NOX2 Complex-Derived ROS as Immune Regulators

被引：160

作者：

Sareila, Outi ^{[1
]}

Kelkka, Tiina ^{[1
,2
,3
]}

Pizzolla, Angela ^{[2
]}

Hultqvist, Malin ^{[4
]}

Holmdahl, Rikard ^{[1
,2
]}

机构：

[1] Univ Turku, MediC Res Lab, FIN-20520 Turku, Finland

[2] Karolinska Inst, Stockholm, Sweden

[3] Turku Grad Sch Biomed Sci TuBS, Turku, Finland

[4] Redoxis AB, Ideon Bioinkubator, Lund, Sweden

来源：

ANTIOXIDANTS & REDOX SIGNALING | 2011年 / 15卷 / 08期

基金：

瑞典研究理事会;

关键词：

SINGLE-NUCLEOTIDE POLYMORPHISM; GENERATING NADPH OXIDASES; REDOX BALANCE ALTERATIONS; REDUCED OXIDATIVE BURST; REACTIVE OXYGEN; RHEUMATOID-ARTHRITIS; SYNOVIAL-FLUID; T-CELLS; VITAMIN-E; P47PHOX PHOSPHORYLATION;

D O I：

10.1089/ars.2010.3635

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Reactive oxygen species (ROS) are a heterogeneous group of highly reactive molecules that oxidize targets in a biologic system. During steady-state conditions, ROS are constantly produced in the electron-transport chain during cellular respiration and by various constitutively active oxidases. ROS production can also be induced by activation of the phagocyte NADPH oxidase 2 (NOX2) complex in a process generally referred to as an oxidative burst. The induced ROS have long been considered proinflammatory, causing cell and tissue destruction. Recent findings have challenged this inflammatory role of ROS, and today, ROS are also known to regulate immune responses and cell proliferation and to determine T-cell autoreactivity. NOX2-derived ROS have been shown to suppress antigen-dependent T-cell reactivity and remarkably to reduce the severity of experimental arthritis in both rats and mice. In this review, we discuss the role of ROS and the NOX2 complex as suppressors of autoimmunity, inflammation, and arthritis. Antioxid. Redox Signal. 15, 2197-2208.

引用

页码：2197 / 2208

页数：12

共 108 条

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