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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

M C Eike^1,2, G B N Nordang^1,2, T H Karlsen^2,3, K M Boberg³, M H Vatn on behalf of the IBSEN study group^3,4, K Dahl-Jørgensen⁵, K S Rønningen⁶, G Joner⁵, B Flatø⁷, A Bergquist⁸, E Thorsby^1,2, Ø Førre⁷, T K Kvien⁹, D E Undlien^10,11, B A Lie¹

¹ Institute of Immunology, Rikshospitalet HF, Oslo, Norway
² Institute of Immunology, Faculty Division Rikshospitalet, University of Oslo, Oslo, Norway
³ Medical Department, Rikshospitalet HF, Oslo, Norway
⁴ EpiGen Akershus University Hospital, University of Oslo, Oslo, Norway
⁵ Department of Paediatrics, Ullevål University Hospital, Oslo, Norway
⁶ Division of Epidemiology, Norwegian Institute of Public Health, Oslo, Norway
⁷ Department of Rheumatology, Rikshospitalet HF, Oslo, Norway
⁸ Department of Gastroenterology and Hepatology, Karolinska University Hospital, Stockholm, Sweden
⁹ Department of Rheumatology, Diakonhjemmet Hospital, Oslo, Norway
¹⁰ Institute of Medical Genetics, University of Oslo, Oslo, Norway
¹¹ Department of Medical Genetics, Ullevål University Hospital, Oslo, Norway

M C Eike, Institute of Immunology, Rikshospitalet HF, N-0027 Oslo, Norway; Morten.Eike{at}rr-research.no

Background and objectives: The Fc receptor-like 3 (FCRL3) gene –169T>C single nucleotide polymorphism (SNP) has been reported to be associated with several autoimmune diseases (AIDs) in Japanese populations. However, association results in other populations have been conflicting. Therefore, we 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 erythaematosus (SLE; n = 166), ulcerative colitis (UC; n = 335), primary sclerosing cholangitis (PSC; n = 365), Crohn disease (CD; n = 149), a healthy control group (n = 1030) and 425 trio families with type 1 diabetes (T1D). Statistical analysis consisted of case–control and family-based association tests.

Results: RA was associated with the C allele (odds ratio (OR) = 1.16, 95% CI 1.01 to 1.33) and the CC genotype (OR = 1.30, 95% CI 1.01 to 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 to 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 patients with RA, 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 titre 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.

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