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Rheumatology Advance Access published online on February 7, 2008
Rheumatology, doi:10.1093/rheumatology/ken005
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© The Author 2008. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Review

Recent advances in the genetics of RA susceptibility

J. Bowes and A. Barton

Arthritis Research Campaign Epidemiology Unit, University of Manchester, Manchester, UK.

Correspondence to: Bowes, ARC-EU, Stopford Building, University of Manchester, Manchester, UK. E-mail: j.bowes{at}manchester.ac.uk


  Abstract

RA is a common autoimmune disease with a complex aetiology in which genetic and environmental factors contribute to disease. The genetic component of RA is largely undefined and, up until very recently, there were only two reproducible associations. The strongest of these associations is of genes within the HLA region, particularly the HLA-DRB1 gene. A second, more modest, association identified has been of the protein tyrosine phosphatase non-receptor 22 (PTPN22) gene. Advances in genotyping technology have facilitated the application of whole genome association approaches to identify disease causal variants. This, coupled with the availability of large case and control collections has enabled the identification of low-to-moderate risk loci. These newer study designs combined with traditional linkage and association studies have accelerated the identification of novel risk loci. The past few months alone have witnessed the identification of three new RA risk loci. In this review, we aim to give an update on recent progress in RA genetics, focusing mainly on the identification of novel loci.

KEY WORDS: Rheumatoid arthritis, GWAS, Candidate, Association, Review

Submitted 16 November 2007; revised version accepted 3 January 2008.
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