Original Article

Genes and Immunity (2013) 14, 234–237; doi:10.1038/gene.2013.12; published online 4 April 2013

No association of primary Sjögren’s syndrome with Fcγ receptor gene variants

K Haldorsen1,2, S Appel1, S Le Hellard3, O Bruland4, J G Brun5, R Omdal6, G Kristjansdottir7, E Theander8, C P D Fernandes3, M Kvarnström9, P Eriksson10, L Rönnblom7, M W Herlenius9, G Nordmark7, R Jonsson1,5 and A I Bolstad2

  1. 1Broegelmann Research Laboratory, The Gade Institute, University of Bergen, Bergen, Norway
  2. 2Department of Clinical Dentistry, University of Bergen, Bergen, Norway
  3. 3Department of Clinical Medicine, University of Bergen, Bergen, Norway
  4. 4Center for Medical Genetics and Molecular Medicine, Haukeland University Hospital, Bergen, Norway
  5. 5Department of Rheumatology, Haukeland University Hospital, Bergen, Norway
  6. 6Clinical Immunology Unit, Department of Internal Medicine, Stavanger University Hospital, Stavanger, Norway
  7. 7Section of Rheumatology, Department of Medical Sciences, Uppsala University, Uppsala, Sweden
  8. 8Department of Rheumatology, Skåne University Hospital, Lund University, Malmö, Sweden
  9. 9Rheumatology Unit, Department of Medicine, Karolinska Institute, Stockholm, Sweden
  10. 10Rheumatology, Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, Linköping, Sweden

Correspondence: Dr K Haldorsen, Broegelmann Research Laboratory, The Gade Institute, University of Bergen Laboratory, Building 5th Floor, Bergen N-5021, Norway. E-mail: kahn@helse-bergen.no

Received 13 December 2012; Revised 20 February 2013; Accepted 22 February 2013
Advance online publication 4 April 2013

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Abstract

The genetic background of primary Sjögren’s syndrome (pSS) is partly shared with systemic lupus erythematosus (SLE). Immunoglobulin G Fc receptors are important for clearance of immune complexes. Fcγ receptor variants and gene deletion have been found to confer SLE risk. In this study, four Fcγ receptor single-nucleotide polymorphisms (SNPs) and one copy number variation (CNV) were studied. Swedish and Norwegian pSS patients (N=527) and controls (N=528) were genotyped for the Fcγ receptor gene variant FCGR2A H131R (rs1801274) by the Illumina GoldenGate assay. FCGR3A F158V (rs396991) was analysed in 488 patients and 485 controls, FCGR3B rs447536 was analysed in 471 patients and 467 controls, and FCGR3B rs448740 was analysed in 478 cases and 455 controls, using TaqMan SNP genotyping assays. FCGR3B CNV was analysed in 124 patients and 139 controls using a TaqMan copy number assay. None of the SNPs showed any association with pSS. Also, no FCGR3B CNV association was detected. The lack of association of pSS with Fcγ receptor gene variants indicates that defective immune complex clearance may not be as important in pSS pathogenesis as in SLE, and may point to important differences between SLE and pSS.

Keywords:

Sjögren’s syndrome; Fc gamma receptors; single-nucleotide polymorphism; DNA copy number variations