| Literature DB >> 28711143 |
Linda T Hiraki1, Earl D Silverman2.
Abstract
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.Entities:
Keywords: Complement deficiency; DNA sensing; Genetics; Interferonopathies; Monogenic diseases; RNA sensing; Systemic lupus erythematosus
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Year: 2017 PMID: 28711143 DOI: 10.1016/j.rdc.2017.04.005
Source DB: PubMed Journal: Rheum Dis Clin North Am ISSN: 0889-857X Impact factor: 2.670