MediCity Research Laboratory, University of Turku, Tykistökatu 6A 4, Turku, Finland.
Antioxid Redox Signal. 2011 Oct 15;15(8):2197-208. doi: 10.1089/ars.2010.3635. Epub 2011 Apr 11.
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.
活性氧（ROS）是一组高度反应性的分子，可氧化生物系统中的靶标。在稳定状态下，ROS 在细胞呼吸的电子传递链中不断产生，并由各种组成性活性氧化酶产生。ROS 的产生也可以通过吞噬细胞 NADPH 氧化酶 2（NOX2）复合物的激活来诱导，这个过程通常被称为氧化爆发。长期以来，诱导产生的 ROS 一直被认为具有促炎作用，导致细胞和组织破坏。最近的研究结果对 ROS 的这种炎症作用提出了挑战，如今，ROS 也被认为可以调节免疫反应、细胞增殖，并决定 T 细胞自身反应性。已经表明，NOX2 衍生的 ROS 可抑制抗原依赖性 T 细胞反应，并显著降低大鼠和小鼠实验性关节炎的严重程度。在这篇综述中，我们讨论了 ROS 和 NOX2 复合物作为自身免疫、炎症和关节炎的抑制剂的作用。
