Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48103-2200, USA.
Cells. 2019 Feb 5;8(2):127. doi: 10.3390/cells8020127.
Lupus flares when genetically predisposed people encounter exogenous agents such as infections and sun exposure and drugs such as procainamide and hydralazine, but the mechanisms by which these agents trigger the flares has been unclear. Current evidence indicates that procainamide and hydralazine, as well as inflammation caused by the environmental agents, can cause overexpression of genes normally silenced by DNA methylation in CD4⁺ T cells, converting them into autoreactive, proinflammatory cytotoxic cells that are sufficient to cause lupus in mice, and similar cells are found in patients with active lupus. More recent studies demonstrate that these cells comprise a distinct CD4⁺ T cell subset, making it a therapeutic target for the treatment of lupus flares. Transcriptional analyses of this subset reveal proteins uniquely expressed by this subset, which may serve as therapeutic to deplete these cells, treating lupus flares.
狼疮在具有遗传易感性的人接触到外源性物质（如感染、阳光暴露和药物，如普鲁卡因胺和肼屈嗪）时会发作，但这些物质引发发作的机制尚不清楚。目前的证据表明，普鲁卡因胺和肼屈嗪以及环境因素引起的炎症，可导致 CD4+T 细胞中正常受 DNA 甲基化沉默的基因过度表达，将其转化为自身反应性、促炎细胞毒性细胞，足以在小鼠中引起狼疮，而在活动性狼疮患者中也发现了类似的细胞。最近的研究表明，这些细胞构成了一个独特的 CD4+T 细胞亚群，使其成为治疗狼疮发作的治疗靶点。对该亚群的转录分析揭示了该亚群特有的表达蛋白，这些蛋白可能作为治疗药物来清除这些细胞，从而治疗狼疮发作。
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