LETTER

Association of IL2RA and IL2RB with rheumatoid arthritis: a replication study in a Dutch population

F A S Kurreeman¹, N A Daha¹, M Chang², J J Catanese², A B Begovich², T W J Huizinga¹, R E M Toes¹

¹ Department of Rheumatology, Leiden University Medical Center, Leiden, The Netherlands
² Celera, Alameda, California, USA

Correspondence to:
^{Correspondence to} Professor R E M Toes, Department of Rheumatology, Leiden University Medical Center, Leiden, The Netherlands; r.e.m.toes@lumc.nl

Accepted 23 February 2009

The first 150 words of the full text of this article appear below.

Rheumatoid arthritis (RA) is an autoimmune disease with a worldwide prevalence of approximately 1%. The aetiology of RA is largely unknown, but it is thought that both genetic and environmental factors play a role in the pathogenesis of the disease. Genome-wide association studies (GWAS) and candidate gene approaches have led to the association of a number of genetic susceptibility loci.^{1 2 3 4 5 6 7} The Wellcome Trust case-control consortium (WTCCC), the first GWAS in RA, identified a number of loci reaching genome-wide significance including the HLA region and the PTPN22 gene.⁵ To identify new genetic risk factors, Thomson et al investigated whether tier 2 single nucleotide polymorphisms (SNPs) (p = 1x10^–5–1x10^–7) in the WTCCC-GWAS showed an association with RA in an independent validation study of 5063 patients and 3849 healthy controls.⁸ Of the nine loci investigated, a significant association was identified with rs6920220 in the TNFAIP3-OLIG3 region (odds . . . [Full text of this article]

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