Hiraki Linda T, Silverman Earl D
Division of Rheumatology, SickKids Hospital, SickKids Research Institute, 555 University Avenue, Toronto, Ontario M5G 1X8, Canada; Department of Paediatrics, University of Toronto, 555 University Avenue, Toronto, Ontario M5G 1X8, Canada; Epidemiology, Dalla Lana School of Public Health, 155 College Street, Toronto, Ontario M5T 3M7, Canada.
Division of Rheumatology, SickKids Hospital, SickKids Research Institute, 555 University Avenue, Toronto, Ontario M5G 1X8, Canada; Department of Paediatrics, University of Toronto, 555 University Avenue, Toronto, Ontario M5G 1X8, Canada; Department of Medicine, University of Toronto, Toronto, Ontario, Canada.
Rheum Dis Clin North Am. 2017 Aug;43(3):415-434. doi: 10.1016/j.rdc.2017.04.005.
Systemic lupus erythematosus (SLE) is a systemic, autoimmune, multisystem disease with a heterogeneous clinical phenotype. Genome-wide association studies have identified multiple susceptibility loci, but these explain a fraction of the estimated heritability. This is partly because within the broad spectrum of SLE are monogenic diseases that tend to cluster in patients with young age of onset, and in families. This article highlights insights into the pathogenesis of SLE provided by these monogenic diseases. It examines genetic causes of complement deficiency, abnormal interferon production, and abnormalities of tolerance, resulting in monogenic SLE with overlapping clinical features, autoantibodies, and shared inflammatory pathways.
系统性红斑狼疮(SLE)是一种具有异质性临床表型的全身性自身免疫性多系统疾病。全基因组关联研究已经确定了多个易感基因座,但这些仅解释了估计遗传力的一部分。部分原因是在SLE的广泛谱系中存在单基因疾病,这些疾病往往在发病年龄较轻的患者中以及在家族中聚集。本文重点介绍了这些单基因疾病为SLE发病机制提供的见解。它研究了补体缺陷、异常干扰素产生和耐受性异常的遗传原因,这些导致了具有重叠临床特征、自身抗体和共享炎症途径的单基因SLE。