title: Humoral beta-cell autoimmunity is rare in patients with the congenital rubella syndrome.
abstract: The congenital rubella syndrome (CRS) is associated with increased risk for diabetes and thyroid disease. However, the mechanisms by which the rubella virus may cause these diseases are poorly characterized. Previous studies were carried out before modern immunological methods were available. The present study aimed at evaluating whether autoimmune mechanisms are involved in the pathogenesis by analysing antibodies to biochemically characterized autoantigens. The incidence of clinical diabetes, thyroid disease, coeliac disease and related antibodies (islet cell antibodies, ICA; insulin autoantibodies, IAA; antibodies to the tyrosine phosphatase related IA-2 molecule, IA-2 A and glutamic acid decarboxylase, GADA; thyroid peroxidase, TPO; tissue transglutaminase, TTGA; and gliadin, AGA) and HLA risk genotypes were analysed in 37 subjects affected by or exposed to rubella during fetal life (mean age 22.5 years). One patient had diabetes and four patients had clinical hypothyroidism at the time of the examination. ICA, IAA, GADA or IA-2 A were not detected in any of the patients, while five patients tested positive for TPO antibodies. Coeliac disease or TTGA were not observed. Eight patients carried the HLA-DR3-associated HLA-DQB1*02-DQA1*05 haplotype. These results provide no evidence of an increased frequency of markers for humoral beta-cell autoimmunity in patients with CRS suggesting that diabetes in CRS may be caused by other than autoimmune mechanisms.
authors.affiliation: JDRF Center for Prevention of Type I Diabetes in Finland, Department of Virology, University of Tampere, Finland. hanna.viskari@uta.fi
authors.forename: H
authors.initials: H
authors.lastname: Viskari
authors.forename: J
authors.initials: J
authors.lastname: Paronen
authors.forename: P
authors.initials: P
authors.lastname: Keskinen
authors.forename: S
authors.initials: S
authors.lastname: Simell
authors.forename: B
authors.initials: B
authors.lastname: Zawilinska
authors.forename: I
authors.initials: I
authors.lastname: Zgorniak-Nowosielska
authors.forename: S
authors.initials: S
authors.lastname: Korhonen
authors.forename: J
authors.initials: J
authors.lastname: Ilonen
authors.forename: O
authors.initials: O
authors.lastname: Simell
authors.forename: A-M
authors.initials: AM
authors.lastname: Haapala
authors.forename: M
authors.initials: M
authors.lastname: Knip
authors.forename: H
authors.initials: H
authors.lastname: Hyöty
mesh_terms: D000328:Adult; D001323:Autoantibodies / Q000097:blood / Q000276:immunology; D015551:Autoimmunity; D001402:B-Lymphocytes / Q000276:immunology*; D015415:Biomarkers / Q000097:blood; D002648:Child; D003920:Diabetes Mellitus / Q000276:immunology; D005260:Female; D019084:Fluorescent Antibody Technique, Indirect; D005838:Genotype; D005903:Gliadin / Q000276:immunology; D005968:Glutamate Decarboxylase / Q000276:immunology; D006683:HLA-DQ Antigens / Q000032:analysis; D059866:HLA-DQ beta-Chains; D006801:Humans; D007037:Hypothyroidism / Q000276:immunology; D007328:Insulin / Q000276:immunology; D007453:Iodide Peroxidase / Q000276:immunology; D007515:Islets of Langerhans / Q000276:immunology; D008297:Male; D012307:Risk Factors; D012410:Rubella Syndrome, Congenital / Q000276:immunology*; D011503:Transglutaminases / Q000276:immunology
chemical_list: D001323:Autoantibodies; D015415:Biomarkers; D006683:HLA-DQ Antigens; D059866:HLA-DQ beta-Chains; C069051:HLA-DQB1 antigen; C096322:ICA512 autoantibody; D007328:Insulin; D005903:Gliadin; D007453:Iodide Peroxidase; D011503:Transglutaminases; D005968:Glutamate Decarboxylase