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Rheumatology Advance Access originally published online on January 30, 2009
Rheumatology 2009 48(4):359-362; doi:10.1093/rheumatology/ken503
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© The Author 2009. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Association of killer cell immunoglobulin-like receptors with primary Sjögren's syndrome

David P. Lowe1, Mark A. Cook2, Simon J. Bowman3, David C. Briggs1 and the UK Sjögren's Interest Group*

1Department of Histocompatibility and Immunogenetics, NHS Blood and Transplant, 2Department of Haematology, University Hospital Birmingham NHS Foundation Trust, Edgbaston, 3Department of Rheumatology, University Hospital Birmingham, NHS Foundation Trust, Birmingham, UK.

Correspondence to: David P. Lowe, Department of Histocompatibility and Immunogenetics, NHS Blood and Transplant, Vincent Drive, Edgbaston, Birmingham B15 2SG, UK. E-mail: dave.lowe{at}nhsbt.nhs.uk


  Abstract

Objective. SS is a chronic inflammatory condition characterized by systemic and tissue-specific autoimmune features. In view of recent findings indicating a role for killer cell immunoglobulin-like receptors (KIRs) in the pathogenesis of other autoimmune rheumatic disorders such as SSc, and the autoimmune disorders RA and PsA, we sought to determine whether KIRs predict general or specific susceptibility in SS.

Methods. Eleven separate KIR genes were typed using PCR sequence-specific primers on genomic DNA from 72 patients diagnosed with primary SS and a control panel consisting of 223 blood donors.

Results. We found no individual KIR genes to be associated with SS. In contrast, 11 patients with primary SS (15%) and 9 control blood donors (4%) had KIR genotypes with the activating KIR2DS2 in the absence of its corresponding inhibitory homologue KIR2DL2 (P = 0.01). Further analysis of these individuals showed that seven SS patients were positive for HLA-C ligand for KIR2DS2 only compared with one control sample (P = 0.00026).

Conclusion. The genetic combination of KIR2DS2+ and KIR2DL2– in the presence of HLA-C ligand specific for activating KIR2DS2 is associated with primary SS. This implies that autologous KIR–ligand interaction is a contributory factor to predisposition for this disease.

KEY WORDS: Killer immunoglobulin-like receptors, SS, Autoimmune disease

*The UK Sjögren's Interest Group includes: Deva Situnayake, Caroline Gordon, Liviu Hanu-Cernat, Stephanie Heaton and Bernard Speculand, City Hospital; John Ainsworth, Ahmed Bawendi and Georgina Holmes, Birmingham Heartlands & Solihull Hospitals; John Hamburger, School of Dentistry, Birmingham; Peter Maddison, Bangor; Diarmuid Mulherin, Cannock Chase Hospital, Staffordshire; Pepe Shirlaw, UMDS, London; Michael Snaith, Mohammed Akil and Christine Yeoman, Royal Hallamshire Hospital, Sheffield; Anne Field, Jocelyn Rostron, Luke Dawson and Leslie Longman, Liverpool Dental Hospital, Liverpool; Ian Griffiths and Brian Davidson, Freeman Hospital, Newcastle; Neil McHugh and Nicola Waldron, Royal National Hospital, Bath; Colin Pease and Elizabeth Tyas, Leeds General Infirmary, Leeds; Elizabeth Price, Princess Margaret Hospital, Swindon; David Isenberg, Maria-Jose Leandro and Nurhan Sutcliffe, Middlesex Hospital, London, UK.

Submitted 9 July 2008; revised version accepted 11 December 2008.
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