A functional variant in FCRL3, encoding Fc receptor-like 3, is associated with rheumatoid arthritis and several
Yuta Kochi1, Ryo Yamada, Akari Suzuki
1Laboratory for Rheumatic Diseases, SNP Research Center, RIKEN, Yokohama 230-0045, Japan.
Abstract:
Rheumatoid arthritis is a common autoimmune disease with a complex genetic etiology. Here we identify a SNP in the promoter region of FCRL3, a member of the Fc receptor-like family, that is associated with susceptibility to rheumatoid arthritis (odds ratio = 2.15, P = 0.00000085). This polymorphism alters the binding affinity of nuclear factor-kappaB and regulates FCRL3 expression. We observed high FCRL3 expression on B cells and augmented autoantibody production in individuals with the disease-susceptible genotype. We also found associations between the SNP and susceptibility to autoimmune thyroid disease and systemic lupus erythematosus. FCRL3 may therefore have a pivotal role in autoimmunity.
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