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Arthritis Research and Therapy

, 8:R117

First Online: 19 July 2006Received: 15 June 2006Revised: 04 July 2006Accepted: 06 July 2006


Association of a functional promoter polymorphism mapping to the Fc receptor-like 3 FCRL3 gene has recently been reported and replicated with rheumatoid arthritis RA in Japanese populations. The aim of this study was to investigate association of the FCRL3 gene with RA in UK subjects. DNA was available from 1065 patients with RA and 2073 population controls from the UK. Four single nucleotide polymorphism SNP markers FCRL3-169*C-T fclr3 3, rs7528684, fclr3 4 rs11264799, fclr3 5 rs945635, fclr3 6 rs3761959 all previously associated with RA in a Japanese population were genotyped in 761 RA samples and 484 controls. In the remaining samples, only the putative disease causal polymorphism, FCRL3-169*C-T, was tested. Genotyping was performed using either the Sequenom MassArray iPlex platform or a 5- Allelic discrimination assay Taqman, ABI. Extensive linkage disequilibrium was present across the promoter SNPs genotyped r values = 0.60-0.98. Allele frequencies did not differ between RA cases and controls either for the putative disease causal polymorphism odds ratio FCRL3-169*C allele = 0.97 0.87-1.07, p = 0.51 or for the other SNPs tested. Similarly, no association was detected with RA using haplotype analysis or when stratification by shared epitope carriage or by presence of rheumatoid factor was undertaken. This study was powered to detect an effect size of 1.24 or greater for the FCRL3-169*C-T functional promoter polymorphism but no evidence for association was detected, suggesting that this gene will not have a substantial effect in determining susceptibility to RA in populations of Northern European descent.

AbbreviationsFCRL3= Fc receptor-like 3

NF= nuclear factor

RA= rheumatoid arthritis

SNP= single nucleotide polymorphism.

An erratum to this article is available at

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Autor: Stephen Eyre - John Bowes - Catherine Potter - Jane Worthington - Anne Barton


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