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The FCRL3 -169T>C polymorphism is associated with rheumatoid arthritis and shows suggestive evidence of involvement with juvenile idiopathic arthritis in a Scandinavian panel of autoimmune diseases.
  1. Morten C Eike (morten.eike{at}
  1. Rikshospitalet HF/University of Oslo, Norway
    1. Gry B N Nordang
    1. Rikshospitalet HF/University of Oslo, Norway
      1. Tom H Karlsen
      1. University of Oslo/Rikshospitalet HF, Norway
        1. Kirsten M Boberg
        1. Rikshospitalet HF, Norway
          1. Morten H Vatn, and the IBSEN study group
          1. Rikshospitalet HF/University of Oslo, Norway
            1. Knut Dahl-Jørgensen
            1. Ullevål University Hospital, Norway
              1. Kjersti S Rønningen
              1. Norwegian Institute of Public Health, Norway
                1. Geir Joner
                1. Ullevål University Hospital, Norway
                  1. Berit Flatø
                  1. Rikshospitalet HF, Norway
                    1. Annika Bergquist
                    1. Karolinska University Hospital, Sweden
                      1. Erik Thorsby
                      1. Rikshospitalet HF/University of Oslo, Norway
                        1. Øystein Førre
                        1. Rikshospitalet HF, Norway
                          1. Tore K Kvien
                          1. Diakonhjemmet Hospital, Norway
                            1. Dag E Undlien
                            1. University of Oslo/Ullevål University Hospital, Norway
                              1. Benedicte A Lie
                              1. Rikshospitalet HF, Norway


                                Background and objectives: The Fc receptor-like 3 (FCRL3) -169T>C single nucleotide polymorphism (SNP) has been reported associated with several autoimmune diseases (AIDs) in Japanese populations. However, association results in other populations have been conflicting. Therefore, we have investigated this SNP in a Scandinavian panel of AIDs.

                                Methods: We genotyped patients with rheumatoid arthritis (RA; n=708), juvenile idiopathic arthritis (JIA; n=524), systemic lupus erythematosus (SLE; n=166), ulcerative colitis (UC; n=335), primary sclerosing cholangitis (PSC; n=365), Crohn’s disease (CD; n=149), a healthy control group (n=1030) and 425 trio families with type 1 diabetes (T1D). Statistical analysis consisted of both case-control and family-based association tests.

                                Results: RA was associated both with the C allele (OR=1.16, 95 % CI 1.01-1.33) and the CC genotype (OR=1.30, 95 % CI 1.01-1.67) of the FCRL3 -169T>C SNP in our material. Suggestive evidence for association was also found for JIA (CC genotype: OR=1.30, 95% CI 0.99-1.70), and clinical subgroup analysis indicated that this was connected to the polyarticular subgroup. No significant association was found with SLE, UC, CD, PSC or T1D. In RA patients, we found no significant interaction between the FCRL3 -169T>C and PTPN22 1858C>T SNPs, nor between the FCRL3 -169CC genotype and IgM-rheumatoid factor or anti-cyclic citrullinated peptide titer levels.

                                Conclusion: We found an association between the FCRL3 -169T>C SNP and RA, and suggestive evidence for involvement with JIA, in a Norwegian population. These findings lend support for a role for this SNP in RA across ethnically diverse populations, and warrant follow-up studies in JIA.

                                • FCRL3
                                • autoimmunity
                                • genetic predisposition
                                • juvenile idiopathic arthritis
                                • rheumatoid arthritis

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