Association of the T-cell regulatory gene CTLA4 with susceptibility to autoimmune disease View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2003-04-30

AUTHORS

Hironori Ueda, Joanna M. M. Howson, Laura Esposito, Joanne Heward, Snook, Giselle Chamberlain, Daniel B. Rainbow, Kara M. D. Hunter, Annabel N. Smith, Gianfranco Di Genova, Mathias H. Herr, Ingrid Dahlman, Felicity Payne, Deborah Smyth, Christopher Lowe, Rebecca C. J. Twells, Sarah Howlett, Barry Healy, Sarah Nutland, Helen E. Rance, Vin Everett, Luc J. Smink, Alex C. Lam, Heather J. Cordell, Neil M. Walker, Cristina Bordin, John Hulme, Costantino Motzo, Francesco Cucca, J. Fred Hess, Michael L. Metzker, Jane Rogers, Simon Gregory, Amit Allahabadia, Ratnasingam Nithiyananthan, Eva Tuomilehto-Wolf, Jaakko Tuomilehto, Polly Bingley, Kathleen M. Gillespie, Dag E. Undlien, Kjersti S. Rønningen, Cristian Guja, Constantin Ionescu-Tîrgovişte, David A. Savage, A. Peter Maxwell, Dennis J. Carson, Chris C. Patterson, Jayne A. Franklyn, David G. Clayton, Laurence B. Peterson, Linda S. Wicker, John A. Todd, Stephen C. L. Gough

ABSTRACT

Genes and mechanisms involved in common complex diseases, such as the autoimmune disorders that affect approximately 5% of the population, remain obscure. Here we identify polymorphisms of the cytotoxic T lymphocyte antigen 4 gene (CTLA4)—which encodes a vital negative regulatory molecule of the immune system—as candidates for primary determinants of risk of the common autoimmune disorders Graves' disease, autoimmune hypothyroidism and type 1 diabetes. In humans, disease susceptibility was mapped to a non-coding 6.1?kb 3′ region of CTLA4, the common allelic variation of which was correlated with lower messenger RNA levels of the soluble alternative splice form of CTLA4. In the mouse model of type 1 diabetes, susceptibility was also associated with variation in CTLA-4 gene splicing with reduced production of a splice form encoding a molecule lacking the CD80/CD86 ligand-binding domain. Genetic mapping of variants conferring a small disease risk can identify pathways in complex disorders, as exemplified by our discovery of inherited, quantitative alterations of CTLA4 contributing to autoimmune tissue destruction. More... »

PAGES

506-511

Journal

TITLE

Nature

ISSUE

6939

VOLUME

423

Author Affiliations

  • Juvenile Diabetes Research Foundation/Wellcome Trust Diabetes and Inflammation Laboratory, Cambridge Institute for Medical Research, University of Cambridge, Wellcome Trust/MRC Building, CB2 2XY, Cambridge, UK
  • Division of Medical Sciences, University of Birmingham, B15 2TT, Birmingham, UK
  • HIT Group, Tenovus Research Laboratories, Southampton General Hospital, Tremona Road, SO16 6YD, Southampton, UK
  • Department of Paediatrics, Otto-Heubner-Centrum, Charité, Humboldt-University of Berlin, Germany
  • Karolinska Institute, Department of Medicine, Huddinge University Hospital, Stockholm, Sweden
  • Dipartimento di Scienze Biomediche e Biotecnologie, Universita di Cagliari, Cagliari, Italy
  • Hutchison/MRC Research Centre, Hills Road, CB2 2XZ, Cambridge, UK
  • Merck Research Laboratories, 19486, West Point, Pennsylvania, USA
  • Department of Molecular & Human Genetics, Baylor Genome Sequencing Center, Baylor College of Medicine, N1409, One Baylor Plaza, 77030, Houston, Texas, USA
  • Wellcome Trust Sanger Institute, CB10 1SA, Cambridge, Hinxton, UK
  • Department of Public Health, University of Helsinki, Helsinki, Finland
  • Division of Clinical Sciences, University of Sheffield, Northern General Hospital, S5 7AU, Sheffield, UK
  • Diabetes and Genetic Epidemiology Unit, National Public Health Institute, University of Helsinki, Helsinki, Finland
  • Diabetes and Metabolism Unit, Division of Medicine, University of Bristol, BS10 5NG, Bristol, UK
  • Institute of Medical Genetics, University of Oslo, N-0315, Oslo, Norway
  • Laboratory of Molecular Epidemiology, Division of Epidemiology, Norwegian Institute of Public Health, Oslo, Norway
  • Clinic of Diabetes, Institute of Diabetes, Nutrition and Metabolic Diseases ‘N. Paulescu’, Bucharest, Romania
  • Department of Medical Genetics, Queen's University Belfast, Belfast City Hospital, BT9 7AB, Belfast, UK
  • Regional Nephrology Unit, Belfast City Hospital, BT9 7AB, Belfast, UK
  • Department of Child Health, Queen's University Belfast, BT12 6BJ, Belfast, UK
  • Department of Epidemiology and Public Health, Queen's University Belfast, BT12 6BJ, Belfast, UK
  • Department of Pharmacology, Merck Research Laboratories, 07065, Rahway, New Jersey, USA
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/nature01621

    DOI

    http://dx.doi.org/10.1038/nature01621

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1004357092

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/12724780


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