Department of Medicine (Solna), Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden; Department of Medical Sciences, Science for Life Laboratory, Uppsala University, Uppsala, Sweden
Lindsey B Rosen
Laboratory of Clinical Immunology & Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, United States
Eva Freyhult
Department of Medical Sciences, National Bioinformatics Infrastructure, Uppsala, Sweden; Science for Life Laboratory, Uppsala University, Uppsala, Sweden
Department of Medicine (Solna), Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden; Department of Endocrinology, Metabolism and Diabetes, Karolinska University Hospital, Stockholm, Sweden
Tove Fall
Department of Medical Sciences, Molecular Epidemiology, Science for Life Laboratory, Uppsala University, Uppsala, Sweden
Gustav Smith
Department of Cardiology, Clinical Sciences, Lund University, Skåne University Hospital, Lund, Sweden; Program in Medical and Population Genetics, Broad Institute of Harvard, Massachusetts Institute of Technology, Cambridge, United States; Wallenberg Center for Molecular Medicine, Lund University Diabetes Center, Lund University, Lund, Sweden
Laboratory of Clinical Immunology & Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, United States
Department of Cardiology, Clinical Sciences, Lund University, Skåne University Hospital, Lund, Sweden; Department of Women's and Children's Health, Science for Life Laboratory, Karolinska Institutet, Stockholm, Sweden; Department of Newborn Medicine, Karolinska University Hospital, Stockholm, Sweden
Donald Sharon
Department of Genetics, School of Medicine, Stanford University, Stanford, United States
Michael Snyder
Wallenberg Center for Molecular Medicine, Lund University Diabetes Center, Lund University, Lund, Sweden; Department of Genetics, School of Medicine, Stanford University, Stanford, United States
Michail Lionakis
Laboratory of Clinical Immunology & Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, United States
Mark Anderson
Diabetes Center, University of California, San Francisco, San Francisco, United States
Department of Medicine (Solna), Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden; Department of Endocrinology, Metabolism and Diabetes, Karolinska University Hospital, Stockholm, Sweden; KG Jebsen Center for Autoimmune Diseases, University of Bergen, Bergen, Norway
The AIRE gene plays a key role in the development of central immune tolerance by promoting thymic presentation of tissue-specific molecules. Patients with AIRE-deficiency develop multiple autoimmune manifestations and display autoantibodies against the affected tissues. In 2016 it was reported that: i) the spectrum of autoantibodies in patients with AIRE-deficiency is much broader than previously appreciated; ii) neutralizing autoantibodies to type I interferons (IFNs) could provide protection against type 1 diabetes in these patients (Meyer et al., 2016). We attempted to replicate these new findings using a similar experimental approach in an independent patient cohort, and found no evidence for either conclusion.
