Department of Rheumatology, Semmelweis University, Medical School, Budapest, Hungary.
Arthritis Res Ther. 2010;12(3):210. doi: 10.1186/ar3045. Epub 2010 Jun 28.
Nitric oxide (NO) has been shown to regulate T cell functions under physiological conditions, but overproduction of NO may contribute to T lymphocyte dysfunction. NO-dependent tissue injury has been implicated in a variety of rheumatic diseases, including systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). Several studies reported increased endogenous NO synthesis in both SLE and RA, and recent evidence suggests that NO contributes to T cell dysfunction in both autoimmune diseases. The depletion of intracellular glutathione may be a key factor predisposing patients with SLE to mitochondrial dysfunction, characterized by mitochondrial hyperpolarization, ATP depletion and predisposition to death by necrosis. Thus, changes in glutathione metabolism may influence the effect of increased NO production in the pathogenesis of autoimmunity.
一氧化氮（NO）已被证明可在生理条件下调节 T 细胞功能，但过量产生的 NO 可能导致 T 淋巴细胞功能障碍。NO 依赖性组织损伤与多种风湿性疾病有关，包括系统性红斑狼疮（SLE）和类风湿关节炎（RA）。多项研究报告称，SLE 和 RA 患者的内源性 NO 合成增加，最近的证据表明，NO 有助于这两种自身免疫性疾病中的 T 细胞功能障碍。细胞内谷胱甘肽的耗竭可能是导致 SLE 患者线粒体功能障碍的关键因素，其特征为线粒体超极化、ATP 耗竭以及容易发生坏死性死亡。因此，谷胱甘肽代谢的变化可能会影响增加的 NO 产生在自身免疫发病机制中的作用。
