Yuta Kochi1, 2, Ryo Yamada1, Akari Suzuki1, John B Harley3, Senji Shirasawa4, Tetsuji Sawada2, Sang-Cheol Bae5, Shinya Tokuhiro1, Xiaotian Chang1, Akihiro Sekine6, Atsushi Takahashi7, Tatsuhiko Tsunoda7, Yozo Ohnishi8, Kenneth M Kaufman3, Changsoo Paul Kang9, Changwon Kang9, Shigeru Otsubo10, Wako Yumura11, Akio Mimori4, Takao Koike12, Yusuke Nakamura10, 13, Takehiko Sasazuki4
& Kazuhiko Yamamoto1, 21
Laboratory for Rheumatic Diseases, SNP Research Center, RIKEN, Yokohama 230-0045, Japan.
2
Department of Allergy and Rheumatology, Graduate School of Medicine, the University of Tokyo, Tokyo 113-0033, Japan.
3
University of Oklahoma; US Department of Veterans Affairs; and Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma 73104, USA.
4
International Medical Center of Japan, Tokyo 162-8655, Japan.
5
Department of Internal Medicine, Division of Rheumatology, the Hospital for Rheumatic Diseases, Hanyang University, Seoul 133-792, Republic of Korea.
6
Laboratory for Genotyping, SNP Research Center, RIKEN, Yokohama 230-0045, Japan.
7
Laboratory for Medical Informatics, SNP Research Center, RIKEN, Yokohama 230-0045, Japan.
8
Laboratory for SNP Analysis, SNP Research Center, RIKEN, Yokohama 230-0045, Japan.
9
Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon 305-701, Republic of Korea.
10
Laboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, the University of Tokyo, Tokyo 108-8639, Japan.
11
Department of Medicine, Kidney Center, Tokyo Women's Medical University, Tokyo 162-8666, Japan.
12
Department of Medicine II, Hokkaido University School of Medicine, Sapporo 060-8638, Japan.
13
Research Group for Personalized Medicine, SNP Research Center, RIKEN, Yokohama 230-0045, Japan.
Correspondence should be addressed to Ryo Yamada ryamada@src.riken.go.jp
B 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.
