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International Journal of Rheumatology
Volume 2012 (2012), Article ID 167096, 4 pages
Research Article

Fc-Gamma Receptor 3B Copy Number Variation Is Not a Risk Factor for Behçet’s Disease

1Department of Rheumatology, The Queen Elizabeth Hospital, 28 Woodville Road, Woodville South, SA, 5011, Australia
2Rheumatology Research Centre, Tehran University of Medical Sciences, Shariati Hospital, Kargar Avenue, Tehran 14114, Iran
3Rheumatology Department, Baqyiatallah University of Medical Sciences, Baghiatallah hospital, Molla Sadra Street, Tehran 14359, Iran
4Chronic Respiratory Diseases Research Centre, Shahid Beheshti University of Medical Sciences, Massih Daneshvari Hospital, Shaid Bahonar Street, Tehran 19556, Iran
5Discipline of Medicine, The University of Adelaide, Adelaide, SA 5005, Australia

Received 13 February 2012; Accepted 10 April 2012

Academic Editor: Lorenzo Beretta

Copyright © 2012 Rachel Black et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Behçet’s disease (BD) is an immune-mediated systemic vasculitis associated with HLAB51. Other gene associations are likely and may provide further insight into the pathogenesis of this disease. Fc-gamma receptors play an important role in regulating immune function. Copy number variation (CNV) of the Fc-gamma receptor 3B (FCGR3B) gene is associated with other inflammatory conditions and may also play a role in BD. The aim of this study was to determine whether CNV of the FCGR3B gene is associated with BD or its clinical features. FCGR3B copy number was determined for 187 Iranian patients and 178 ethnicity-matched controls using quantitative real-time PCR. The genotype frequencies were comparable in both BD patients and controls. The odds ratio for low copy number (<2CN) was 0.6 ( 𝑃 = 0 . 1 6 ) and the odds ratio for high copy number (>2CN) was 0.75 ( 𝑃 = 0 . 5 0 ). There was no association found between high or low CN of the FCGR3B gene and BD or its clinical features in this Iranian population. We are the first to report this finding which, when looked at in the context of other genetic studies, gives us further insight into the complex pathogenesis of BD.