FCGR3B copy number variation is associated with susceptibility to systemic, but not organ-specific, autoimmunity View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2007-06

AUTHORS

Manuela Fanciulli, Penny J Norsworthy, Enrico Petretto, Rong Dong, Lorraine Harper, Lavanya Kamesh, Joanne M Heward, Stephen C L Gough, Adam de Smith, Alexandra I F Blakemore, Philippe Froguel, Catherine J Owen, Simon H S Pearce, Luis Teixeira, Loic Guillevin, Deborah S Cunninghame Graham, Charles D Pusey, H Terence Cook, Timothy J Vyse, Timothy J Aitman

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 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. More... »

PAGES

721-723

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ng2046

DOI

http://dx.doi.org/10.1038/ng2046

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1039814739

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/17529978


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