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Kochi, Yuta,Yamada, Ryo,Suzuki, Akari,Harley, John B,Shirasawa, Senji,Sawada, Tetsuji,Bae, Sang-Cheol,Tokuhiro, Shinya,Chang, Xiaotian,Sekine, Akihiro,Takahashi, Atsushi,Tsunoda, Tatsuhiko,Ohnishi, Yo Nature Publishing Group 2005 Nature genetics Vol.37 No.5
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-κB 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.