Journal
EXPERT REVIEW OF CLINICAL IMMUNOLOGY
Volume 6, Issue 3, Pages 461-479Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1586/ECI.10.8
Keywords
genome-wide association studies; pathogenesis; systemic lupus erythematosus; Toll-like receptor signaling; type I interferon signaling
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Funding
- NIH [R01 AR052300, R01 AR22804, P60 AR053308, K24 AR02175, M01 RR-00079]
- Kirkland Scholar Award
- Alliance for Lupus Research
- NATIONAL CENTER FOR RESEARCH RESOURCES [M01RR000079] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR052300, R01AR044804, P60AR053308, K24AR002175] Funding Source: NIH RePORTER
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Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by the production of antinuclear autoantibodies and the inflammatory infiltration of many organ systems. SLE is a complex disorder in which multiple genetic variants, together with environmental and hormonal factors, contribute to disease risk. In this article, we summarize our current understanding of the genetic contribution to SLE in light of recent genome-wide association studies, which have brought the total number of confirmed SLE susceptibility loci to 29. In the second section, we explore the functional implications of these risk loci and, in particular, highlight the role that many of these genes play in the Toll-like receptor and type I interferon signaling pathways. Finally, we discuss the genetic overlap between SLE and other autoimmune and inflammatory conditions as several risk loci are shared among multiple disorders, suggesting common underlying pathogenic mechanisms.
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