Journal article
High-density genetic mapping identifies new susceptibility loci for rheumatoid arthritis
S Eyre, J Bowes, D Diogo, A Lee, A Barton, P Martin, A Zhernakova, E Stahl, S Viatte, K McAllister, CI Amos, L Padyukov, REM Toes, TWJ Huizinga, C Wijmenga, G Trynka, L Franke, HJ Westra, L Alfredsson, X Hu Show all
Nature Genetics | Published : 2012
DOI: 10.1038/ng.2462
Abstract
Using the Immunochip custom SNP array, which was designed for dense genotyping of 186 loci identified through genome-wide association studies (GWAS), we analyzed 11,475 individuals with rheumatoid arthritis (cases) of European ancestry and 15,870 controls for 129,464 markers. We combined these data in a meta-analysis with GWAS data from additional independent cases (n = 2,363) and controls (n = 17,872). We identified 14 new susceptibility loci, 9 of which were associated with rheumatoid arthritis overall and five of which were specifically associated with disease that was positive for anticitrullinated peptide antibodies, bringing the number of confirmed rheumatoid arthritis risk loci in ind..
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Awarded by Arthritis Foundation
Funding Acknowledgements
We thank). Barrett and C. Wallace for the SNP selection. We thank the Wellcome Trust Sanger Institute Genotyping Facility, and, in particular, E. Gray, S. Bumpstead, D. Simpkin and H. Blackburn. Genotyping of the UK Rheumatoid Arthritis Genetics samples was supported by the Arthritis Research UK grant reference number 17552 and the Manchester Biomedical Research Centre. This work was made possible by funds from the Arthritis Foundation (S.R., principal investigator) and the US National Institutes Health (K08AR055688 to S.R. and 1R01AR062886-01 to P.I.W.d.B). P. Gilbert prepared the UK samples. Genotyping of the Swedish Umea samples was performed by the SNP&SEQ Technology Platform in Uppsala, which is supported by Uppsala University, Uppsala University Hospital, Science for Life Laboratory-Uppsala and the Swedish Research Council (contracts 80576801 and 70374401). This work was partially supported by the Redes Tematicas de Investigacion Cooperative en Salud (RETICS) Program, RD08/0075 (RIER), from the Instituto de Salud Carlos III, Spain. We acknowledge use of DNA from the UK Blood Services collection of Common Controls (UKBS-CC collection), which is funded by Wellcome Trust grant 076113/C/04/Z and by the US National Institutes for Health research program grant to the National Health Service Blood and Transplant (RP-PG-0310-1002). We acknowledge the use of DNA from the British 1958 Birth Cohort collection, which is funded by the UK Medical Research Council grant G0000934 and the Wellcome Trust grant 068545/Z/02. The North American Rheumatoid Arthritis Consortium and analysis of other US patient and control collections at the Feinstein Institute were supported by the US National Institutes of Health RO1-AR-4-4422, NO1-AR-2-2263; NO1-AR1-2256, RO1 AI068759 and RC2AR059092-01, with additional support from the Eileen Ludwig Greenland Center for Rheumatoid Arthritis and the family of Robert S. Boas. R.M.P. is supported by grants from the US National Institutes of Health (R01-AR057108, R01-AR056768, U01-GM092691 and R01-AR059648) and holds a Career Award for Medical Scientists from the Burroughs Wellcome Fund.