| pubmed-article:17529978 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17529978 | lifeskim:mentions | umls-concept:C0012655 | lld:lifeskim |
| pubmed-article:17529978 | lifeskim:mentions | umls-concept:C0205419 | lld:lifeskim |
| pubmed-article:17529978 | lifeskim:mentions | umls-concept:C0004368 | lld:lifeskim |
| pubmed-article:17529978 | lifeskim:mentions | umls-concept:C0332281 | lld:lifeskim |
| pubmed-article:17529978 | lifeskim:mentions | umls-concept:C1414556 | lld:lifeskim |
| pubmed-article:17529978 | lifeskim:mentions | umls-concept:C0205373 | lld:lifeskim |
| pubmed-article:17529978 | lifeskim:mentions | umls-concept:C1707513 | lld:lifeskim |
| pubmed-article:17529978 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:17529978 | pubmed:dateCreated | 2007-5-30 | lld:pubmed |
| pubmed-article:17529978 | pubmed:abstractText | 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. | lld:pubmed |
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| pubmed-article:17529978 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17529978 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17529978 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:17529978 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17529978 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:17529978 | pubmed:issn | 1061-4036 | lld:pubmed |
| pubmed-article:17529978 | pubmed:author | pubmed-author:FroguelPhilip... | lld:pubmed |
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| pubmed-article:17529978 | pubmed:author | pubmed-author:HewardJoanne... | lld:pubmed |
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| pubmed-article:17529978 | pubmed:author | pubmed-author:de SmithAdamA | lld:pubmed |
| pubmed-article:17529978 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17529978 | pubmed:volume | 39 | lld:pubmed |
| pubmed-article:17529978 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17529978 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17529978 | pubmed:pagination | 721-3 | lld:pubmed |
| pubmed-article:17529978 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:17529978 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17529978 | pubmed:articleTitle | FCGR3B copy number variation is associated with susceptibility to systemic, but not organ-specific, autoimmunity. | lld:pubmed |
| pubmed-article:17529978 | pubmed:affiliation | Physiological Genomics and Medicine Group, UK Medical Research Council (MRC) Clinical Sciences Centre, Imperial College, London W12 0NN, UK. | lld:pubmed |
| pubmed-article:17529978 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17529978 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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