| Literature DB >> 12192244 |
Jim C Oates1, Gary S Gilkeson.
Abstract
Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterized by the production of autoantibodies and the development of immune complex glomerulonephritis. Lupus nephritis (LN) remains a leading cause of morbidity and mortality in SLE. As a result, defining pathogenetic mediators in LN remains a major research effort. Progression to LN in SLE is dependent on the host breaking immune tolerance and forming autoantibodies that deposit in the kidney. A variety of predisposing factors in the host must then be present for this event to result in renal pathology. In this article, the authors review recent reports that advance our understanding of LN disease mediators, from autoantibody production and immune complex deposition to end stage fibrosis.Entities:
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Year: 2002 PMID: 12192244 DOI: 10.1097/00002281-200209000-00003
Source DB: PubMed Journal: Curr Opin Rheumatol ISSN: 1040-8711 Impact factor: 5.006