Whole genome association study results shed light on elusive aetiopathogenesis of systemic lupus erythematosus.
Whole genome association study results shed light on elusive aetiopathogenesis of systemic lupus erythematosus.
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全基因组关联研究结果揭示了系统性红斑狼疮难以捉摸的发病机制。
DOI：
10.1111/j.1742-1241.2008.01745.x
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发表时间：
2008
影响因子：
2.6
通讯作者：
Costenbader,KH
中科院分区：
文献类型：
--
作者：
Kyttaris,VC;Costenbader,KH
导致系统性红斑狼疮(SLE)发展的事件在很大程度上仍然难以捉摸。外界因素，如病毒和内源性分子，如激素，被假定导致遗传易感人群的疾病发展[在(1)中回顾]。然而，遗传、表观遗传和环境因素的确切贡献以及它们如何相互作用尚不清楚。在病理生理学水平上(2)，临床SLE的发展是一个两步过程。首先，在正常情况下阻止自身免疫的耐受机制无法阻止自身反应细胞的产生，或者无法抑制它们的功能。这些自身反应细胞，包括B细胞和T细胞，可能在临床症状出现前几年出现在SLE患者的血液和组织中，在疾病发作前9年的血清中检测到自身抗体就证明了这一点。疾病发病机制的第二步是自身抗体、免疫复合物和异常激活的免疫细胞渗入靶器官，导致系统性红斑狼疮的各种临床表现，如肾炎、关节炎和皮炎。
The events that lead to the development of systemic lupus erythematosus (SLE) remain largely elusive. External factors, such as viruses, and endogenous molecules, such as hormones, are hypothesised to lead to the development of the disease in the genetically predisposed person [reviewed in (1)]. Nevertheless, the exact contributions of genetic, epigenetic and environmental factors and how they interact are not understood. On a pathophysiological level (2), clinical SLE develops as a two-step process. First, the tolerance mechanisms that under normal conditions prevent autoimmunity fail to prevent the generation of autoreactive cells or fail to suppress their function. These autoreactive cells, both B and T cells, may be present in the blood and tissues of patients with SLE years before the emergence of clinical symptoms, attested to by the detection of autoantibodies in the sera up to 9 years before disease onset (3). The second step in disease pathogenesis occurs when autoantibodies, immune complexes and abnormally activated immune cells infiltrate target organs, leading to the various clinical manifestations of SLE such as nephritis, arthritis and dermatitis.