title: No evidence of abnormal regulation of antibody response to coxsackievirus B4 antigen in prediabetic children.
abstract: Enterovirus infections are a potential environmental trigger of the autoimmune process leading to clinical type 1 diabetes. It has been suggested that the risk of virus-induced beta-cell damage might be connected with a defect in humoral immune responsiveness to enteroviruses. In the present study we assessed whether such a defect in IgG responsiveness to coxsackievirus B4 antigen existed in young children who developed diabetes-associated autoantibodies during prospective observation from birth until the age of 18 months. IgG levels and maturation of antibody avidity were analysed in 21 children with autoantibodies and 41 control children who had experienced an equal number of enterovirus infections and were additionally matched for age, sex and HLA-DQB1 risk alleles for type 1 diabetes but had not produced diabetes-associated autoantibodies. IgG levels to coxsackievirus B4 were high in cord serum reflecting the presence of maternal antibodies. Mean IgG levels gradually decreased but began to increase after the age of 6 months, showing no significant difference between autoantibody positive and control children. The avidity of antibodies was strong in cord serum and decreased gradually during the first year of life when maternal antibodies disappeared. The avidity indices, which varied considerably from child to child, did not differ between the autoantibody-positive and -negative subjects. In conclusion, our data suggest that children affected by a beta-cell damaging autoimmune process show normal responses to coxsackievirus B4 antigens.
authors.affiliation: JDRF-Centre for the Prevention of Type 1 Diabetes in Finland, Tampere, Finland.
authors.forename: L
authors.initials: L
authors.lastname: Heino
authors.forename: M
authors.initials: M
authors.lastname: Lönnrot
authors.forename: M
authors.initials: M
authors.lastname: Knip
authors.forename: A
authors.initials: A
authors.lastname: Kupila
authors.forename: S
authors.initials: S
authors.lastname: Erkkilä
authors.forename: A
authors.initials: A
authors.lastname: Toivonen
authors.forename: P
authors.initials: P
authors.lastname: Vähäsalo
authors.forename: J
authors.initials: J
authors.lastname: Ilonen
authors.forename: O
authors.initials: O
authors.lastname: Simell
authors.forename: H
authors.initials: H
authors.lastname: Hyöty
mesh_terms: D000914:Antibodies, Viral / Q000097:blood*; D000915:Antibody Affinity; D000956:Antigens, Viral; D001323:Autoantibodies / Q000097:blood; D016022:Case-Control Studies; D003922:Diabetes Mellitus, Type 1 / Q000209:etiology / Q000235:genetics / Q000276:immunology* / Q000821:virology*; D029822:Enterovirus B, Human / Q000276:immunology* / Q000472:pathogenicity; D005260:Female; D005312:Fetal Blood / Q000276:immunology; D006683:HLA-DQ Antigens / Q000235:genetics; D059866:HLA-DQ beta-Chains; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood*; D007223:Infant; D007231:Infant, Newborn; D008297:Male; D011236:Prediabetic State / Q000209:etiology / Q000235:genetics / Q000276:immunology* / Q000821:virology*; D011446:Prospective Studies
chemical_list: D000914:Antibodies, Viral; D000956:Antigens, Viral; D001323:Autoantibodies; D006683:HLA-DQ Antigens; D059866:HLA-DQ beta-Chains; C069051:HLA-DQB1 antigen; D007074:Immunoglobulin G