A functional variant in FCRL3, encoding Fc receptor-like 3, is associated with rheumatoid arthritis and several autoimmunities

Yuta Kochi, Ryo Yamada, Akari Suzuki, John B. Harley, Senji Shirasawa, Tetsuji Sawada, Sang Cheol Bae, Shinya Tokuhiro, Xiaotian Chang, Akihiro Sekine, Atsushi Takahashi, Tatsuhiko Tsunoda, Yozo Ohnishi, Kenneth M. Kaufman, Changsoo Paul Kang, Changwon Kang, Shigeru Otsubo, Wako Yumura, Akio Mimori, Takao KoikeYusuke Nakamura, Takehiko Sasazuki, Kazuhiko Yamamoto

研究成果: Contribution to journalArticle査読

297 被引用数 (Scopus)

抄録

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-ê 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.

本文言語英語
ページ(範囲)478-485
ページ数8
ジャーナルNature genetics
37
5
DOI
出版ステータス出版済み - 5 2005
外部発表はい

All Science Journal Classification (ASJC) codes

  • Genetics

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