FCGR3B copy number variation is associated with susceptibility to systemic, but not organ-specific, autoimmunity.
FCGR3B copy number variation is associated with susceptibility to systemic, but not organ-specific, autoimmunity.
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天然发生的基因拷贝数变化越来越多地被认为是对遗传复杂疾病的敏感性的来源。 = 2.9×10-4）和来自英国两个独立队列（p = 3×10-3）和法国（p = 1.1×× 10-4）。
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.
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