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The role of nitric oxide in abnormal T cell signal transduction in systemic lupus erythematosus.

机译:一氧化氮在系统性红斑狼疮异常T细胞信号转导中的作用。

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摘要

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by production of antinuclear autoantibodies and diverse array of clinical manifestations. T cells from patients with SLE have been shown to be activated in vivo and provide help to autoreactive B cells. Lupus T cells exhibit enhanced spontaneous and diminished activation-induced apoptosis and predisposition to necrosis. Persistent mitochondrial hyperpolarization and ATP depletion - associated with significantly increased mitochondrial mass - characterize T lymphocyte dysfunction in SLE. In addition to cell death abnormalities, mitochondrial dysfunction is associated with altered signal transduction through the T cell receptor and Ca2+ fluxing. Exposure of normal T cell to nitric oxide induces mitochondrial hyperpolarization and biogenesis and regenerates the Ca2+ signaling profile of lupus T cells. This article reviews a novel understanding of the role of nitric oxide in signal transduction and cell death abnormalities in SLE.
机译:系统性红斑狼疮(SLE)是一种慢性自身免疫性疾病,其特征是产生抗核自身抗体和多种临床表现。 SLE患者的T细胞已被证明在体内被激活,并为自身反应性B细胞提供帮助。狼疮T细胞表现出增强的自发性和减弱的激活诱导的细胞凋亡和易坏死的倾向。持续性线粒体超极化和ATP耗竭(与线粒体质量显着增加有关)是SLE中T淋巴细胞功能障碍的特征。除细胞死亡异常外,线粒体功能障碍还与通过T细胞受体和Ca2 +通量改变的信号传导有关。正常T细胞暴露于一氧化氮会诱导线粒体超极化和生物发生,并重新生成狼疮T细胞的Ca2 +信号传导特征。本文回顾了对一氧化氮在SLE中信号转导和细胞死亡异常中的作用的新颖理解。

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