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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

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.

https://doi.org/10.1136/ard.2008.095927

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    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.