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Analysis of association of DNASE2 promoter variation with rheumatoid arthritis in European Caucasians
  1. Amanda Phipps-Green1,
  2. Cushla McKinney1,
  3. Manuela Rossol2,
  4. Marilyn E Merriman1,
  5. Ruth Topless1,
  6. Jade E Hollis-Moffatt1,
  7. Wan Rohani Wan Taib1,
  8. Nicola Dalbeth3,
  9. Peter J Gow4,
  10. Andrew A Harrison5,
  11. John Highton6,
  12. Peter B B Jones3,
  13. Lisa K Stamp7,
  14. Ulf Wanger2,
  15. Paul Wordsworth8,
  16. Tony R Merriman1
  1. 1Department of Biochemistry, University of Otago, Dunedin, New Zealand
  2. 2Department of Internal Medicine II, Division of Rheumatology, University of Leipzig, Leipzig, Germany
  3. 3Department of Medicine, University of Auckland, Auckland, New Zealand
  4. 4Department of Rheumatology, Middlemore Hospital, Auckland, New Zealand
  5. 5Department of Medicine, University of Otago, Wellington, New Zealand
  6. 6Department of Medicine, University of Otago, Dunedin, New Zealand
  7. 7Department of Medicine, University of Otago, Christchurch, New Zealand
  8. 8Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Nuffield Orthopaedic Centre, University of Oxford, Oxford, UK
  1. Correspondence to Tony R Merriman, Department of Biochemistry, University of Otago, Box 56, Dunedin 9054, New Zealand; tony.merriman{at}otago.ac.nz

https://doi.org/10.1136/ard.2010.138727

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    Deoxyribonuclease II (DNASE2) is a lysosomal enzyme responsible for degrading DNA released from cells during erythropoiesis or apoptosis.1 DNASE2 mouse knockouts develop chronic polyarthritis similar to human rheumatoid arthritis (RA), including rheumatoid factor (RF).2 Association has been reported between three single nucleotide polymorphisms (SNPs; rs11085823, rs12609744 and rs249143) in tight linkage disequilibrium within the DNASE2 promoter and RA in German Caucasian samples, with differential association according to RF status.3

    With the aim of replicating the previous findings,3 rs12609744, chosen because HapMap data were available for imputation, was genotyped using a TaqMan assay (Applied Biosystems, Foster City, California, USA) in New Zealand and UK Caucasian case-control samples,4 5 and imputed genotype data retrieved from a genome-wide scan (table 1).6 No evidence for association was found in any of the sample sets (OR 0.93–0.99, p=0.27–0.97) (table 1). In meta-analysis using a …

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    Footnotes

    • Funding Health Research Council of New Zealand, Arthritis New Zealand, University of Oxford

    • Competing interests None.

    • Ethical approval Ethical approval for the study in New Zealand was given by the New Zealand Multi-region Ethics Committee and the Lower South Ethics Committee, and in the UK by the Oxford Research Ethics Committee. All subjects gave written informed consent.

    • Provenance and peer review Not commissioned; externally peer reviewed.

    • The first two authors contributed equally to this work.