期刊
NATURE GENETICS
卷 39, 期 6, 页码 721-723出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ng2046
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资金
- Medical Research Council [MC_U120061454, MC_U120097112] Funding Source: Medline
- Medical Research Council [MC_U120097112, G0000934, G84/5959, G0400116, MC_U120061454] Funding Source: Medline
- Wellcome Trust [068545/Z/02, 066780] Funding Source: Medline
- Medical Research Council [G0400116, G0000934, G84/5959] Funding Source: researchfish
- Medical Research Council [MC_U120061454] Funding Source: researchfish
- MRC [G84/5959, G0400116, G0000934, MC_U120061454] Funding Source: UKRI
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 x 10(-8)), microscopic polyangiitis (P = 2.9 x 10(-4)) and Wegener's granulomatosis in two independent cohorts from the UK ( P = 3 x 10(-3)) and France ( P = 1.1 x 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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