title: Anti-transglutaminase antibodies in non-coeliac children suffering from infectious diseases.
abstract: Anti-transglutaminase antibodies are the diagnostic markers of coeliac disease. A role is suggested for infectious agents in the production of anti-transglutaminase antibodies. The aim was to measure positive anti-transglutaminase antibody levels in children with infectious diseases and to compare immunological and biological characteristics of the anti-transglutaminase antibodies derived from these children with that from coeliac patients. Two hundred and twenty-two children suffering from infectious diseases were enrolled prospectively along with seven biopsy-proven coeliacs. Serum samples were tested for anti-transglutaminase antibodies and anti-endomysium antibodies; positive samples were tested for coeliac-related human leucocyte antigen (HLA)-DQ2/8 and anti-viral antibodies. Purified anti-transglutaminase antibodies from the two study groups were tested for urea-dependent avidity, and their ability to induce cytoskeletal rearrangement and to modulate cell-cycle in Caco-2 cells, using phalloidin staining and bromodeoxyuridine incorporation assays, respectively. Nine of 222 children (4%) tested positive to anti-transglutaminase, one of whom also tested positive for anti-endomysium antibodies. This patient was positive for HLA-DQ2 and was diagnosed as coeliac following intestinal biopsy. Of the eight remaining children, two were positive for HLA-DQ8. Levels of anti-transglutaminase returned to normal in all subjects, despite a gluten-containing diet. Purified anti-transglutaminase of the two study groups induced actin rearrangements and cell-cycle progression. During an infectious disease, anti-transglutaminase antibodies can be produced temporarily and independently of gluten. The infection-triggered anti-transglutaminase antibodies have the same biological properties as that of the coeliacs, with the same in-vivo potential for damage.
authors.affiliation: Department of Reproductive and Development Science, University of Trieste, and Children Hospital IRCCS 'Burlo Garofolo' Trieste, Italy.
authors.forename: F
authors.initials: F
authors.lastname: Ferrara
authors.forename: S
authors.initials: S
authors.lastname: Quaglia
authors.forename: I
authors.initials: I
authors.lastname: Caputo
authors.forename: C
authors.initials: C
authors.lastname: Esposito
authors.forename: M
authors.initials: M
authors.lastname: Lepretti
authors.forename: S
authors.initials: S
authors.lastname: Pastore
authors.forename: R
authors.initials: R
authors.lastname: Giorgi
authors.forename: S
authors.initials: S
authors.lastname: Martelossi
authors.forename: G
authors.initials: G
authors.lastname: Dal Molin
authors.forename: N
authors.initials: N
authors.lastname: Di Toro
authors.forename: A
authors.initials: A
authors.lastname: Ventura
authors.forename: T
authors.initials: T
authors.lastname: Not
mesh_terms: D000199:Actins / Q000378:metabolism; D000293:Adolescent; D000906:Antibodies / Q000494:pharmacology; D001323:Autoantibodies / Q000097:blood / Q000276:immunology*; D018938:Caco-2 Cells; D002446:Celiac Disease / Q000097:blood / Q000175:diagnosis / Q000276:immunology*; D002453:Cell Cycle / Q000187:drug effects; D002648:Child; D002675:Child, Preschool; D003141:Communicable Diseases / Q000097:blood / Q000175:diagnosis / Q000276:immunology*; D003599:Cytoskeleton / Q000187:drug effects / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D008297:Male; D008856:Microscopy, Fluorescence; D011446:Prospective Studies; D011503:Transglutaminases / Q000276:immunology*
chemical_list: D000199:Actins; D000906:Antibodies; D001323:Autoantibodies; D011503:Transglutaminases