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- Title
FCGR3B copy number variation is associated with susceptibility to systemic, but not organ-specific, autoimmunity.
- Authors
Fanciulli, Manuela; Norsworthy, Penny J.; Petretto, Enrico; Dong, Rong; Harper, Lorraine; Kamesh, Lavanya; Heward, Joanne M.; Gough, Stephen C. L.; de Smith, Adam; Blakemore, Alexandra I. F.; Froguel, Philippe; Owen, Catherine J.; Pearce, Simon H. S.; Teixeira, Luis; Guillevin, Loic; Cunninghame Graham, Deborah S.; Pusey, Charles D.; Cook, H. Terence; Vyse, Timothy J.; Aitman, Timothy J.
- Abstract
Naturally occurring variation in gene copy number is increasingly recognized as a heritable source of susceptibility to genetically complex diseases. Here we report strong association between FCGR3B copy number and risk of systemic lupus erythematosus (P = 2.7 × 10−8), microscopic polyangiitis (P = 2.9 × 10−4) and Wegener's granulomatosis in two independent cohorts from the UK (P = 3 × 10−3) and France (P = 1.1 × 10−4). We did not observe this association in the organ-specific Graves' disease or Addison's disease. Our findings suggest that low FCGR3B copy number, and in particular complete FCGR3B deficiency, has a key role in the development of systemic autoimmunity.
- Subjects
HUMAN genetics; GENETICS; SYSTEMIC lupus erythematosus; GRANULOMATOSIS with polyangiitis; AUTOIMMUNE diseases
- Publication
Nature Genetics, 2007, Vol 39, Issue 6, p721
- ISSN
1061-4036
- Publication type
Article
- DOI
10.1038/ng2046