title: A functional variant in FCRL3, encoding Fc receptor-like 3, is associated with rheumatoid arthritis and several autoimmunities.
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.
authors.affiliation: Laboratory for Rheumatic Diseases, SNP Research Center, RIKEN, Yokohama 230-0045, Japan.
authors.forename: Yuta
authors.initials: Y
authors.lastname: Kochi
authors.forename: Ryo
authors.initials: R
authors.lastname: Yamada
authors.forename: Akari
authors.initials: A
authors.lastname: Suzuki
authors.forename: John B
authors.initials: JB
authors.lastname: Harley
authors.forename: Senji
authors.initials: S
authors.lastname: Shirasawa
authors.forename: Tetsuji
authors.initials: T
authors.lastname: Sawada
authors.forename: Sang-Cheol
authors.initials: SC
authors.lastname: Bae
authors.forename: Shinya
authors.initials: S
authors.lastname: Tokuhiro
authors.forename: Xiaotian
authors.initials: X
authors.lastname: Chang
authors.forename: Akihiro
authors.initials: A
authors.lastname: Sekine
authors.forename: Atsushi
authors.initials: A
authors.lastname: Takahashi
authors.forename: Tatsuhiko
authors.initials: T
authors.lastname: Tsunoda
authors.forename: Yozo
authors.initials: Y
authors.lastname: Ohnishi
authors.forename: Kenneth M
authors.initials: KM
authors.lastname: Kaufman
authors.forename: Changsoo Paul
authors.initials: CP
authors.lastname: Kang
authors.forename: Changwon
authors.initials: C
authors.lastname: Kang
authors.forename: Shigeru
authors.initials: S
authors.lastname: Otsubo
authors.forename: Wako
authors.initials: W
authors.lastname: Yumura
authors.forename: Akio
authors.initials: A
authors.lastname: Mimori
authors.forename: Takao
authors.initials: T
authors.lastname: Koike
authors.forename: Yusuke
authors.initials: Y
authors.lastname: Nakamura
authors.forename: Takehiko
authors.initials: T
authors.lastname: Sasazuki
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Yamamoto
mesh_terms: D001172:Arthritis, Rheumatoid / Q000235:genetics* / Q000276:immunology / Q000378:metabolism; D015551:Autoimmunity / Q000235:genetics* / Q000276:immunology / Q000502:physiology; D016022:Case-Control Studies; D002878:Chromosomes, Human, Pair 1; D005786:Gene Expression Regulation / Q000502:physiology; D006684:HLA-DR Antigens / Q000235:genetics / Q000276:immunology; D059811:HLA-DRB1 Chains; D006801:Humans; D015810:Linkage Disequilibrium; D008969:Molecular Sequence Data; D005810:Multigene Family; D009154:Mutation; D020641:Polymorphism, Single Nucleotide; D011971:Receptors, Immunologic / Q000235:genetics* / Q000378:metabolism
chemical_list: C457775:FCRL3 protein, human; D006684:HLA-DR Antigens; D059811:HLA-DRB1 Chains; D011971:Receptors, Immunologic