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Review

Genetic epidemiology: Systemic lupus erythematosus

Yasmeen A Ahmad and Ian N Bruce*

Author Affiliations

University of Manchester Rheumatism Research Centre, Central Manchester and Manchester Children's University NHS Trust, Manchester, UK

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Arthritis Res 2001, 3:331-336  doi:10.1186/ar324

Published: 23 August 2001

Abstract

Systemic lupus erythematosus is the prototype multisystem autoimmune disease. A strong genetic component of susceptibility to the disease is well established. Studies of murine models of systemic lupus erythematosus have shown complex genetic interactions that influence both susceptibility and phenotypic expression. These models strongly suggest that several defects in similar pathways, e.g. clearance of immune complexes and/or apoptotic cell debris, can all result in disease expression. Studies in humans have found linkage to several overlapping regions on chromosome 1q, although the precise susceptibility gene or genes in these regions have yet to be identified. Recent studies of candidate genes, including Fcγ receptors, IL-6, and tumour necrosis factor-α, suggest that in human disease, genetic factors do play a role in disease susceptibility and clinical phenotype. The precise gene or genes involved and the strength of their influence do, however, appear to differ considerably in different populations.

Keywords:
candidate genes; disease susceptibility; linkage analysis; mouse models; SLE