rss
Ann Rheum Dis 2009;68:595-598 doi:10.1136/ard.2008.095927
  • Basic and translational research

Analysis of killer immunoglobulin-like receptor genes in ankylosing spondylitis

  1. D Harvey1,
  2. J J Pointon1,
  3. C Sleator2,
  4. A Meenagh2,
  5. C Farrar1,
  6. J Y Sun3,
  7. D Senitzer3,
  8. D Middleton2,
  9. M A Brown1,4,
  10. B P Wordsworth1
  1. 1
    Institute of Musculoskeletal Sciences, Botnar Research Centre, University of Oxford, Oxford, UK
  2. 2
    Northern Ireland Regional Histocompatibility and Immunogenetics Laboratory, City Hospital, Belfast, UK
  3. 3
    Division of Haematology and Bone Marrow Transplantation, City of Hope National Medical Centre, Duaete, California, USA
  4. 4
    Diamantina Institute of Cancer, Immunology and Metabolic Medicine, University of Queensland, Brisbane, Australia
  1. Professor B P Wordsworth, Nuffield Department of Orthopaedic Surgery, Nuffield Orthopaedic Centre, Windmill Road, Headington, Oxford OX3 7LD, UK; Paul.Wordsworth{at}ndm.ox.ac.uk
  • Accepted 29 October 2008
  • Published Online First 19 November 2008

Abstract

Objectives: To assess the possible association of killer immunoglobulin-like receptor (KIR) genes, specifically KIR3DL1, KIR3DS1 and KIR3DL2, with ankylosing spondylitis (AS).

Methods: 14 KIR genes were genotyped in 200 UK patients with AS and 405 healthy controls using multiplex polymerase chain reaction. Sequence-specific oligonucleotide probes were used to subtype 368 cases with AS and 366 controls for 12 KIR3DL2 alleles. Differences in KIR genotypes and KIR3DL2 allele frequencies were assessed using the χ2 test.

Results: KIR3DL1 and KIR3DS1 gene frequencies were very similar in cases with AS and controls (odds ratio = 1.5, 95% confidence interval 0.8 to 3.0, and odds ratio = 1.02, 95% confidence interval 0.2 to 5.3, respectively). KIR3DL2 allele frequencies were not significantly different between cases with AS and controls.

Conclusions: Neither the KIR gene content of particular KIR haplotypes nor KIR3DL2 polymorphisms contribute to AS.

Footnotes

  • Competing interests: None.

  • Funding: DH is funded by the Arthritis Research Campaign (UK). The authors are grateful for additional financial support from the National Ankylosing Spondylitis Society.

This Article

  1. Abstract
  2. Full text
  3. PDF
  4. All versions of this article:
    1. ard.2008.095927v1
    2. ard.2008.095927v2
    3. 68/4/595 most recent

Responses

  1. Submit a response
  2. No responses published

Register for free content

The full back archive is now available for all BMJ Journals. Institutional subscribers may access the entire archive as part of their subscription. Personal subscribers will also have access to all content when logged in. Non-subscribers who register have free access to all articles published before 2006 right back to volume 1 issue 1. Register here to access the free archive of all BMJ Journals.

Don't forget to sign up for content alerts so you keep up to date with all the articles as they are published.