title: Low prevalence of IgA anti-transglutaminase 1, 2, and 3 autoantibodies in children with atopic dermatitis.
abstract: BACKGROUND
  Atopic dermatitis (AD) is a multifactorial chronic inflammatory skin disease presenting with a relapsing clinical pattern similar to chronic autoimmune disease. Several human transglutaminases have been defined and keratinocyte transglutaminase (TG1) and epidermal transglutaminase (TG3) expressed in the epidermis are associated with epidermal barrier dysfunction. Since impairments to the epidermal barrier represent an important factor in AD, we hypothesized that IgA autoantibodies specific for TG1 (IgA-anti-TG1) and TG3 (IgA-anti-TG3) may affect AD development during childhood.
  
  
  METHODS
  Active AD patients (n = 304), 28 patients with biopsy-confirmed coeliac disease (CD), 5 patients with active AD and CD, and 55 control patients without CD and skin diseases were enrolled into the study. IgA-anti-TG1 and IgA-anti-TG3 reactivity was determined using an enzyme-linked immunosorbent assay. IgA-anti-TG2 were defined using a fluoroenzyme immunoassay.
  
  
  RESULTS
  IgA-anti-TG1 antibodies were found in 2% and IgA-anti-TG3 antibodies in 3% of patients with active AD. Two out of the 5 patients with AD and concomitant CD had IgA-anti-TG1 and IgA-anti-TG2 antibodies. In CD patients, 36% of individuals presented with elevated IgA-anti-TG1 antibodies and 18% presented with elevated IgA-anti-TG3 antibodies and all CD patients presented with IgA-anti-TG2 antibodies (significantly different from AD patients and controls, p < 0.05). In CD patients, IgA-anti-TG1 and/or IgA-anti-TG3 seropositivity tended to appear concurrently, whereas only one patient with AD had both types of autoantibodies.
  
  
  CONCLUSIONS
  IgA-anti-TG1 and IgA-anti-TG3 seropositivity was rare in active AD but frequent in CD patients. The level of circulating antibodies related to skin lesions could be studied by determining the levels of IgA-anti-TG1 and IgA-anti-TG3 in skin biopsies of AD patients.
authors.forename: Krista
authors.initials: K
authors.lastname: Ress
authors.forename: Kaupo
authors.initials: K
authors.lastname: Teesalu
authors.forename: Triine
authors.initials: T
authors.lastname: Annus
authors.forename: Urve
authors.initials: U
authors.lastname: Putnik
authors.forename: Kristi
authors.initials: K
authors.lastname: Lepik
authors.forename: Katrin
authors.initials: K
authors.lastname: Luts
authors.forename: Oivi
authors.initials: O
authors.lastname: Uibo
authors.affiliation: Department of Immunology, Institute of Bio- and Translational Medicine and Centre of Excellence for Translational Medicine, University of Tartu, Ravila 19, 50411 Tartu, Estonia. raivo.uibo@ut.ee.
authors.forename: Raivo
authors.initials: R
authors.lastname: Uibo
mesh_terms: D001323:Autoantibodies / Q000097:blood / Q000276:immunology*; D002446:Celiac Disease / Q000276:immunology; D002648:Child; D002675:Child, Preschool; D003876:Dermatitis, Atopic / Q000097:blood / Q000276:immunology*; D005260:Female; D019204:GTP-Binding Proteins / Q000276:immunology; D006801:Humans; D007070:Immunoglobulin A / Q000276:immunology*; D008297:Male; D015995:Prevalence; D000091345:Protein Glutamine gamma Glutamyltransferase 2; D011503:Transglutaminases / Q000276:immunology*
chemical_list: D001323:Autoantibodies; D007070:Immunoglobulin A; D000091345:Protein Glutamine gamma Glutamyltransferase 2; C498712:TGM3 protein, human; D011503:Transglutaminases; C105804:transglutaminase 1; D019204:GTP-Binding Proteins