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Oxidative T Cell Modifications in Lupus and Sjogren’s Syndrome

机译:狼疮和干燥综合征中的氧化性T细胞修饰

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摘要

ObjectivesLupus flares are triggered by environmental agents that cause oxidative stress, but the mechanisms involved are unclear. The flares are characterized by oxidative modifications of proteins by 4-hydroxynonenals, malondialdehydes, carbonyls and nitration. These modifications have been proposed to induce and perpetuate lupus flares by “altered self” mechanisms. An epigenetically altered CD4+CD28+ T cell subset, caused at least in part by nitration of T cell signaling molecules, is found in patients with active lupus, and nitrated T cells are sufficient to cause lupus-like autoimmunity in animal models. The relation of protein 4-hydroxynonenals, malondialdehydes, carbonyls and nitration to lupus flares though, is unknown. We tested if the size of the epigenetically altered subset is related to disease activity and one or more of these oxidative modifications in lupus patients. We also tested the relationship between subset size, disease activity and the same oxidative modifications in Sjogren’s syndrome, another autoimmune disease also associated with oxidative stress and characterized by anti-nuclear antibodies and the presence of the subset.
机译:目的狼疮耀斑是由引起氧化应激的环境因素触发的,但其机制尚不清楚。耀斑的特征在于通过4-羟基壬烯醛,丙二醛,羰基和硝化作用对蛋白质进行氧化修饰。已经提出了这些修饰,以通过“改变的自我”机制诱导和维持狼疮的发作。在患有活动性狼疮的患者中发现表观遗传改变的CD4 + CD28 + T细胞亚群至少部分是由T细胞信号分子的硝化引起的,而硝化的T细胞足以在动物模型中引起类似狼疮的自身免疫。蛋白质4-羟基壬烯醛,丙二醛,羰基和硝化与狼疮耀斑的关系尚不清楚。我们测试了表观遗传改变的子集的大小是否与疾病活动以及狼疮患者中的一种或多种这些氧化修饰有关。我们还测试了子集大小,疾病活动性和干燥综合征中相同的氧化修饰之间的关系,该综合征是另一种自身免疫性疾病,也与氧化应激相关,并具有抗核抗体和该子集的存​​在。

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