Fine-mapping and functional studies highlight potential causal variants for rheumatoid arthritis and type 1 diabetes

Harm-Jan Westra, Marta Martinez-Bonet, Suna Onengut-Gumuscu, Annette Lee, Yang Luol, Nikola Teslovich, Jane Worthington, Javier Martin, Tom Huizinga, Lars Klareskog, Solbritt Rantapaa-Dahlqvist, Wei-Min Chen, Aaron Quinlan, John A. Todd, Steve Eyre, Peter A. Nigrovic, Peter K. G. Regersen, Stephen S. Rich, Soumya Raychaudhuri*

*Corresponding author for this work

    Research output: Contribution to journalArticleAcademicpeer-review

    38 Citations (Scopus)

    Abstract

    To define potentially causal variants for autoimmune disease, we fine-mapped(1,2) 76 rheumatoid arthritis (11,475 cases,15,870 controls)(3) and type 1 diabetes loci (9,334 cases, 11,111 controls)(4). After sequencing 799 1-kilobase regulatory (H3K4me3) regions within these loci in 568 individuals, we observed accurate imputation for 89% of common variants. We defined credible sets of

    Original languageEnglish
    Pages (from-to)1366-1374
    Number of pages12
    JournalNature Genetics
    Volume50
    Issue number10
    DOIs
    Publication statusPublished - Oct-2018

    Keywords

    • GENOME-WIDE ASSOCIATION
    • SYSTEMIC-LUPUS-ERYTHEMATOSUS
    • INFLAMMATORY-BOWEL-DISEASE
    • BURROWS-WHEELER TRANSFORM
    • SUSCEPTIBILITY LOCI
    • CELL-TYPES
    • TYROSINE-PHOSPHATASE
    • GENOTYPE IMPUTATION
    • COMPLEX TRAIT
    • RISK LOCI

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