title: Lack of a role for cross-reacting anti-thyroid antibodies in chronic idiopathic urticaria.
abstract: The etiology of chronic idiopathic urticaria (CIU) is attributed to autoantibodies directed against the alpha-chain of the high-affinity IgE receptor (FcepsilonRIalpha) or IgE on mast cells in 30-60% of patients. Approximately 30% of CIU patients have Hashimoto's thyroiditis (HT). We investigated the pathophysiologic relationship of anti-thyroid and anti-FcepsilonRIalpha antibodies. Nine individuals with both CIU and HT underwent autologous serum skin testing (ASST) and sera were assayed for thyroid autoantibodies, thyroid-stimulating hormone, and anti-FcepsilonRIalpha antibodies. Serum samples were studied for their ability to activate a human mast cell line (LUVA) as determined by cysteinyl leukotriene (CysLT) production. Experiments were performed to determine whether epitope cross-reactivity could explain the high incidence of HT found in CIU patients. A significant proportion of CIU patients had a positive ASST (nine of six) and anti-FcepsilonRIalpha antibodies (six of nine). Incubation of patient sera with FcepsilonRIalpha, but not thyroglobulin or thyroid peroxidase, resulted in the decreased ability to detect anti-FcepsilonRIalpha antibodies. Incubation with thyroid antigens did not inhibit CysLT production by mast cells. Epitopic cross-reactivity does not explain the increased prevalence of HT found in CIU patients. The frequent concurrence of HT and CIU likely reflects a genetic tendency toward autoimmune diseases.
authors.affiliation: Asthma and Allergic Disease Center, Carter Center for Immunology Research, University of Virginia, Charlottesville, Virginia, USA.
authors.forename: Jonathan D
authors.initials: JD
authors.lastname: Mozena
authors.forename: Adrienne
authors.initials: A
authors.lastname: Tiñana
authors.forename: Julie
authors.initials: J
authors.lastname: Negri
authors.forename: John W
authors.initials: JW
authors.lastname: Steinke
authors.forename: Larry
authors.initials: L
authors.lastname: Borish
mesh_terms: D000328:Adult; D000368:Aged; D001323:Autoantibodies / Q000097:blood / Q000276:immunology; D002460:Cell Line; D002908:Chronic Disease; D003429:Cross Reactions / Q000276:immunology; D000939:Epitopes / Q000276:immunology; D005260:Female; D050031:Hashimoto Disease / Q000453:epidemiology / Q000235:genetics / Q000276:immunology*; D006801:Humans; D007073:Immunoglobulin E / Q000276:immunology*; D007453:Iodide Peroxidase / Q000276:immunology*; D008297:Male; D008407:Mast Cells / Q000166:cytology / Q000276:immunology; D008875:Middle Aged; D017455:Receptors, IgE / Q000276:immunology*; D016036:Seroepidemiologic Studies; D013954:Thyroglobulin / Q000276:immunology*; D014581:Urticaria / Q000453:epidemiology / Q000235:genetics / Q000276:immunology*
chemical_list: D001323:Autoantibodies; D000939:Epitopes; C543355:FcepsilonRI alpha-chain, human; D017455:Receptors, IgE; C006606:anti-thyroglobulin; D007073:Immunoglobulin E; D013954:Thyroglobulin; D007453:Iodide Peroxidase