title: Fine mapping in the MHC region accounts for 18% additional genetic risk for celiac disease.
abstract: Although dietary gluten is the trigger for celiac disease, risk is strongly influenced by genetic variation in the major histocompatibility complex (MHC) region. We fine mapped the MHC association signal to identify additional risk factors independent of the HLA-DQA1 and HLA-DQB1 alleles and observed five new associations that account for 18% of the genetic risk. Taking these new loci together with the 57 known non-MHC loci, genetic variation can now explain up to 48% of celiac disease heritability.
authors.affiliation: Department of Genetics, University Medical Center, University of Groningen, Groningen, the Netherlands.
authors.forename: Javier
authors.initials: J
authors.lastname: Gutierrez-Achury
authors.affiliation: Department of Genetics, University Medical Center, University of Groningen, Groningen, the Netherlands.
authors.forename: Alexandra
authors.initials: A
authors.lastname: Zhernakova
authors.affiliation: Department of Medical Genetics, Center for Molecular Medicine, University Medical Center Utrecht, Utrecht, the Netherlands.
authors.forename: Sara L
authors.initials: SL
authors.lastname: Pulit
authors.affiliation: Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Cambridge, UK.
authors.forename: Gosia
authors.identifier: 0000000269559529
authors.initials: G
authors.lastname: Trynka
authors.affiliation: Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
authors.forename: Karen A
authors.initials: KA
authors.lastname: Hunt
authors.affiliation: Department of Genetics, University Medical Center, University of Groningen, Groningen, the Netherlands.
authors.forename: Jihane
authors.initials: J
authors.lastname: Romanos
authors.affiliation: 1] Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA. [2] Division of Genetics, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA. [3] Program in Medical and Population Genetics, Broad Institute, Cambridge, Massachusetts, USA. [4] Arthritis Research UK Epidemiology Unit, Centre for Musculoskeletal Research, Institute of Inflammation and Repair, University of Manchester, Manchester, UK.
authors.forename: Soumya
authors.initials: S
authors.lastname: Raychaudhuri
authors.affiliation: Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
authors.forename: David A
authors.identifier: 0000000206372265
authors.initials: DA
authors.lastname: van Heel
authors.affiliation: Department of Genetics, University Medical Center, University of Groningen, Groningen, the Netherlands.
authors.forename: Cisca
authors.initials: C
authors.lastname: Wijmenga
authors.affiliation: 1] Department of Medical Genetics, Center for Molecular Medicine, University Medical Center Utrecht, Utrecht, the Netherlands. [2] Department of Epidemiology, Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, the Netherlands.
authors.forename: Paul I W
authors.identifier: 0000000177357858
authors.initials: PI
authors.lastname: de Bakker
mesh_terms: D016022:Case-Control Studies; D002446:Celiac Disease / Q000235:genetics*; D002874:Chromosome Mapping; D056726:Genetic Association Studies; D020022:Genetic Predisposition to Disease; D059848:HLA-DQ alpha-Chains / Q000235:genetics*; D059866:HLA-DQ beta-Chains / Q000235:genetics*; D006239:Haplotypes; D006801:Humans; D012306:Risk; D012307:Risk Factors
chemical_list: D059848:HLA-DQ alpha-Chains; D059866:HLA-DQ beta-Chains; C069050:HLA-DQA1 antigen; C069051:HLA-DQB1 antigen