Ikari K, Momohara S, Nakamura T, Hara M, Yamanaka H, Tomatsu T, Kamatani N
Institute of Rheumatology, Tokyo Women's Medical University, 10-22 Kawada, Shinjuku, Tokyo 162-0054, Japan.
Ann Rheum Dis. 2006 May;65(5):671-3. doi: 10.1136/ard.2005.043489. Epub 2005 Sep 21.
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.
To validate the findings of this previous report by examining the -169C-->T single nucleotide polymorphism (SNP) in a large cohort.
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 chi(2) testing.
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).
This result supports a genetic association of the FCRL3 promoter polymorphism with rheumatoid arthritis.
在日本人群中,已报道类风湿关节炎易感性与Fc受体样3基因(FCRL3)之间存在关联。一项病例对照研究表明,该关联的最有力证据源自FCRL3启动子区域的一种多态性,其对该基因的表达具有调控作用。
通过检测一大群人中的-169C→T单核苷酸多态性(SNP)来验证该先前报告的结果。
对752例无亲缘关系的病例和940例对照进行基因分型。所有样本与原研究来自相同种族背景。使用5'等位基因鉴别分析进行基因分型。通过卡方检验检测类风湿关节炎易感性与-169C→T SNP之间的关联。
与先前研究一样,该SNP在病例组和对照组之间显示出显著差异(p = 0.022,优势比 = 1.18,95%置信区间1.02至1.35)。
该结果支持FCRL3启动子多态性与类风湿关节炎之间的遗传关联。