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Supportive evidence for a genetic association of the FCRL3 promoter polymorphism with rheumatoid arthritis
  1. K Ikari,
  2. S Momohara,
  3. T Nakamura,
  4. M Hara,
  5. H Yamanaka,
  6. T Tomatsu,
  7. N Kamatani
  1. Institute of Rheumatology, Tokyo Women’s Medical University, Tokyo, Japan
  1. Correspondence to:
    Dr Katsunori Ikari
    Institute of Rheumatology, Tokyo Women’s Medical University, 10-22 Kawada, Shinjuku, Tokyo 162-0054, Japan; kikari{at}ior.twmu.ac.jp

Abstract

Background: An association between susceptibility to rheumatoid arthritis and the Fc receptor-like 3 gene (FCRL3) has been reported in a Japanese population. A case–control study showed that the strongest evidence of the association was derived from a polymorphism in the promoter region of FCRL3, which has a regulatory effect on the expression of the gene.

Objective: To validate the findings of this previous report by examining the −169C→T single nucleotide polymorphism (SNP) in a large cohort.

Methods: 752 unrelated cases and 940 controls were genotyped. All the samples were from the same ethnic background as the original study. Genotyping was done using 5′ allelic discrimination assays. Association between susceptibility to rheumatoid arthritis and −169C→T SNP was examined by χ2 testing.

Results: As in the previous study, the SNP showed significant differences between cases and controls (p = 0.022, odds ratio = 1.18, 95% confidence interval 1.02 to 1.35).

Conclusions: This result supports a genetic association of the FCRL3 promoter polymorphism with rheumatoid arthritis.

  • RF, rheumatoid factor
  • SNP, single nucleotide polymorphism
  • rheumatoid arthritis
  • FCRL3
  • rheumatoid factor
  • replication

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Footnotes

  • Published Online First 21 September 2005

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