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  • Lenz, Tobias L. (author)

Widespread non-additive and interaction effects within HLA loci modulate the risk of autoimmune diseases

  • Article/chapterEnglish2015

Publisher, publication year, extent ...

  • 2015-08-10
  • Macmillan Publishers Ltd.2015
  • printrdacarrier

Numbers

  • LIBRIS-ID:oai:DiVA.org:umu-109376
  • https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-109376URI
  • https://doi.org/10.1038/ng.3379DOI
  • http://kipublications.ki.se/Default.aspx?queryparsed=id:131933968URI

Supplementary language notes

  • Language:English
  • Summary in:English

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  • Subject category:ref swepub-contenttype
  • Subject category:art swepub-publicationtype

Notes

  • Human leukocyte antigen (HLA) genes confer substantial risk for autoimmune diseases on a log-additive scale. Here we speculated that differences in autoantigen-binding repertoires between a heterozygote's two expressed HLA variants might result in additional non-additive risk effects. We tested the non-additive disease contributions of classical HLA alleles in patients and matched controls for five common autoimmune diseases: rheumatoid arthritis (n(cases) = 5,337), type 1 diabetes (T1D; n(cases) = 5,567), psoriasis vulgaris (n(cases) = 3,089), idiopathic achalasia (n(cases) = 727) and celiac disease (ncases = 11,115). In four of the five diseases, we observed highly significant, non-additive dominance effects (rheumatoid arthritis, P = 2.5 x 10(-12); T1D, P = 2.4 x 10(-10); psoriasis, P = 5.9 x 10(-6); celiac disease, P = 1.2 x 10(-87)). In three of these diseases, the non-additive dominance effects were explained by interactions between specific classical HLA alleles (rheumatoid arthritis, P = 1.8 x 10(-3); T1D, P = 8.6 x 10(-27); celiac disease, P = 6.0 x 10(-100)). These interactions generally increased disease risk and explained moderate but significant fractions of phenotypic variance (rheumatoid arthritis, 1.4%; T1D, 4.0%; celiac disease, 4.1%) beyond a simple additive model.

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  • Deutsch, Aaron J. (author)
  • Han, Buhm (author)
  • Hu, Xinli (author)
  • Okada, Yukinori (author)
  • Eyre, Stephen (author)
  • Knapp, Michael (author)
  • Zhernakova, Alexandra (author)
  • Huizinga, Tom W. J. (author)
  • Abecasis, Goncalo (author)
  • Becker, Jessica (author)
  • Boeckxstaens, Guy E. (author)
  • Chen, Wei-Min (author)
  • Franke, Andre (author)
  • Gladman, Dafna D. (author)
  • Gockel, Ines (author)
  • Gutierrez-Achury, Javier (author)
  • Martin, Javier (author)
  • Nair, Rajan P. (author)
  • Noethen, Markus M. (author)
  • Onengut-Gumuscu, Suna (author)
  • Rahman, Proton (author)
  • Rantapää-Dahlqvist, Solbritt,1947-Umeå universitet,Reumatologi(Swepub:umu)sora0001 (author)
  • Stuart, Philip E. (author)
  • Tsoi, Lam C. (author)
  • van Heel, David A. (author)
  • Worthington, Jane (author)
  • Wouters, Mira M. (author)
  • Klareskog, LarsKarolinska Institutet (author)
  • Elder, James T. (author)
  • Gregersen, Peter K. (author)
  • Schumacher, Johannes (author)
  • Rich, Stephen S. (author)
  • Wijmenga, Cisca (author)
  • Sunyaev, Shamil R. (author)
  • de Bakker, Paul I. W. (author)
  • Raychaudhuri, Soumya (author)
  • Umeå universitetReumatologi (creator_code:org_t)

Related titles

  • In:Nature Genetics: Macmillan Publishers Ltd.47:9, s. 1085-10901061-40361546-1718

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