Pathogenesis of systemic lupus erythematosus (SLE)

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Presentation transcript:

Pathogenesis of systemic lupus erythematosus (SLE) Pathogenesis of systemic lupus erythematosus (SLE). Genes confirmed in more than one genome-wide association analysis in northern European whites (several confirmed in Asians as well) as increasing susceptibility to SLE or lupus nephritis are listed (reviewed in SG Guerra et al: Arthritis Res Ther 14:211, 2012). Gene-environment interactions (reviewed in KH Costenbader et al: Autoimmune Rev 11:604, 2012) result in abnormal immune responses that generate pathogenic autoantibodies and immune complexes that deposit in tissue, activate complement, cause inflammation, and over time lead to irreversible organ damage (reviewed in GC Tsokos: N Engl J Med 365:2110, 2011; and BH Hahn, in DJ Wallace, BH Hahn [eds]: Dubois’ Lupus Erythematosus and Related Syndromes, 8th ed. New York, Elsevier, 2013). Ag, antigen; C1q, complement system; C3, complement component; CNS, central nervous system; DC, dendritic cell; EBV, Epstein-Barr virus; HLA, human leukocyte antigen; FcR, immunoglobulin Fc-binding receptor; IL, interleukin; MCP, monocyte chemotactic protein; PTPN, phosphotyrosine phosphatase; UV, ultraviolet. Source: Systemic Lupus Erythematosus, Harrison's Principles of Internal Medicine, 19e Citation: Kasper D, Fauci A, Hauser S, Longo D, Jameson J, Loscalzo J. Harrison's Principles of Internal Medicine, 19e; 2015 Available at: http://accessmedicine.mhmedical.com/DownloadImage.aspx?image=/data/books/1130/kas_ch378_f001.png&sec=98729457&BookID=1130&ChapterSecID=79749933&imagename= Accessed: October 29, 2017 Copyright © 2017 McGraw-Hill Education. All rights reserved