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


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2015-09

AUTHORS

Tobias L Lenz, Aaron J Deutsch, Buhm Han, Xinli Hu, Yukinori Okada, Stephen Eyre, Michael Knapp, Alexandra Zhernakova, Tom W J Huizinga, Gonçalo Abecasis, Jessica Becker, Guy E Boeckxstaens, Wei-Min Chen, Andre Franke, Dafna D Gladman, Ines Gockel, Javier Gutierrez-Achury, Javier Martin, Rajan P Nair, Markus M Nöthen, Suna Onengut-Gumuscu, Proton Rahman, Solbritt Rantapää-Dahlqvist, Philip E Stuart, Lam C Tsoi, David A van Heel, Jane Worthington, Mira M Wouters, Lars Klareskog, James T Elder, Peter K Gregersen, Johannes Schumacher, Stephen S Rich, Cisca Wijmenga, Shamil R Sunyaev, Paul I W de Bakker, Soumya Raychaudhuri

ABSTRACT

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 (ncases = 5,337), type 1 diabetes (T1D; ncases = 5,567), psoriasis vulgaris (ncases = 3,089), idiopathic achalasia (ncases = 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 × 10(-12); T1D, P = 2.4 × 10(-10); psoriasis, P = 5.9 × 10(-6); celiac disease, P = 1.2 × 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 × 10(-3); T1D, P = 8.6 × 10(-27); celiac disease, P = 6.0 × 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. More... »

PAGES

1085-1090

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ng.3379

DOI

http://dx.doi.org/10.1038/ng.3379

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1018131274

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/26258845


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640 National Institute for Health Research (NIHR) Manchester Musculoskeletal Biomedical Research Unit, Central Manchester University Hospitals National Health Service (NHS) Foundation Trust, Manchester Academic Health Sciences Centre, Manchester, UK.
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643 schema:name Blizard Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
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654 schema:name Department of Human Genetics and Disease Diversity, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
655 Division of Genetics, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts, USA.
656 Division of Medical Sciences, Harvard Medical School, Boston, Massachusetts, USA.
657 Division of Rheumatology, Immunology and Allergy, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts, USA.
658 Laboratory for Statistical Analysis, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.
659 Partners Center for Personalized Genetic Medicine, Boston, Massachusetts, USA.
660 Program in Medical and Population Genetics, Broad Institute, Cambridge, Massachusetts, USA.
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662 https://www.grid.ac/institutes/grid.7692.a schema:alternateName University Medical Center Utrecht
663 schema:name Department of Epidemiology, University Medical Center Utrecht, Utrecht, the Netherlands.
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666 https://www.grid.ac/institutes/grid.9764.c schema:alternateName Kiel University
667 schema:name Institute of Clinical Molecular Biology, Kiel University, Kiel, Germany.
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