Medical Inflammation Research, MBB, Karolinska Institutet, Stockholm, Sweden.
Antioxid Redox Signal. 2013 Apr 20;18(12):1463-74. doi: 10.1089/ars.2012.4734. Epub 2012 Aug 17.
An unexpected finding, revealed by positional cloning of genetic polymorphisms controlling models for rheumatoid arthritis, exposed a new function of Ncf1 and NADPH oxidase (NOX) 2 controlled oxidative burst.
A decreased capacity to produce ROS due to a natural polymorphism was found to be the major factor leading to more severe arthritis and increased T cell-dependent autoimmunity.
In the vein of this finding, we here review a possible new role of ROS in regulating inflammatory cell and autoreactive T cell activity. It is postulated that peroxide is an immunologic transmitter secreted by antigen-presenting cells that downregulate the responses by autoreactive T cells.
This may operate at different levels of T cell selection and activation: during negative selection in the thymus, priming of T cells in draining lymph nodes, and while interacting with macrophages in peripheral target tissues.
通过对控制类风湿关节炎模型的遗传多态性进行定位克隆，揭示了一个意外的发现，即 Ncf1 和 NADPH 氧化酶 (NOX) 2 控制的氧化爆发的新功能。
由于自然多态性导致产生 ROS 的能力下降，被发现是导致更严重关节炎和增加 T 细胞依赖性自身免疫的主要因素。
基于这一发现，我们在这里回顾了 ROS 在调节炎症细胞和自身反应性 T 细胞活性方面的一个可能的新作用。据推测，过氧化物是一种由抗原呈递细胞分泌的免疫递质，可下调自身反应性 T 细胞的反应。
这可能在 T 细胞选择和激活的不同水平上起作用：在胸腺中的阴性选择、引流淋巴结中 T 细胞的启动，以及与外周靶组织中的巨噬细胞相互作用时。
