title: Tissue transglutaminase ELISA positivity in autoimmune disease independent of gluten-sensitive disease.
abstract: BACKGROUND
  Our aim was to understand why some sera from patients with a broad spectrum of autoimmune diseases or non-autoimmune diseases involving enhanced apoptosis, cell lysis and/or putative secondary autoimmune processes show reactions in the tissue transglutaminase (TGc) ELISA used for diagnosis of gluten-sensitive disease.
  
  
  METHODS
  Sera were compared from groups of patients with autoimmune diseases, diseases involving organ specific enhanced cell death, celiac disease or dermatitis herpetiformis, diseases of non-autoimmune origin, and a group without known disease. IgA antibodies against TGc were detected using human antigen (produced recombinantly in bacterial or human cells) in different systems (non-commercial ELISA with buffers of differing NaCl concentrations, and anti-TGc sandwich ELISA). Anti-gliadin and anti-endomysium antibodies were also determined.
  
  
  RESULTS
  Many sera from patients with autoimmune disorders gave a positive signal in the human TGc ELISAs. The signal appeared related to minor impurities in the recombinant human TGc used and to raised serum IgA antibody levels rather than to the occurrence of TGc specific antibodies in these patients.
  
  
  CONCLUSIONS
  No association of anti-TGc Abs and autoimmune conditions independent of gluten-sensitive disease could be shown. Care should be taken to exclude copurification of chaperones, like heat shock protein 70, where preparing antigens for TGc ELISAs.
authors.affiliation: Department of Dermato-Venereology and -Oncology, Semmelweis University, H-1085 Budapest, Mária u. 41., Hungary. sardym@mail.nih.gov
authors.forename: Miklós
authors.initials: M
authors.lastname: Sárdy
authors.forename: Márta
authors.initials: M
authors.lastname: Csikós
authors.forename: Christof
authors.initials: C
authors.lastname: Geisen
authors.forename: Klaudia
authors.initials: K
authors.lastname: Preisz
authors.forename: Zoltán
authors.initials: Z
authors.lastname: Kornseé
authors.forename: Erika
authors.initials: E
authors.lastname: Tomsits
authors.forename: Ulrich
authors.initials: U
authors.lastname: Töx
authors.forename: Nicolas
authors.initials: N
authors.lastname: Hunzelmann
authors.forename: Jörgen
authors.initials: J
authors.lastname: Wieslander
authors.forename: Sarolta
authors.initials: S
authors.lastname: Kárpáti
authors.forename: Mats
authors.initials: M
authors.lastname: Paulsson
authors.forename: Neil
authors.initials: N
authors.lastname: Smyth
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001323:Autoantibodies / Q000097:blood; D001327:Autoimmune Diseases / Q000175:diagnosis / Q000201:enzymology* / Q000276:immunology*; D002446:Celiac Disease / Q000175:diagnosis / Q000201:enzymology* / Q000276:immunology*; D002648:Child; D004797:Enzyme-Linked Immunosorbent Assay / Q000379:methods / Q000592:standards*; D005189:False Positive Reactions; D005260:Female; D019204:GTP-Binding Proteins / Q000276:immunology*; D006801:Humans; D007070:Immunoglobulin A / Q000097:blood; D007223:Infant; D008297:Male; D008875:Middle Aged; D000091345:Protein Glutamine gamma Glutamyltransferase 2; D015203:Reproducibility of Results; D012680:Sensitivity and Specificity; D011503:Transglutaminases / Q000276:immunology*
chemical_list: D001323:Autoantibodies; D007070:Immunoglobulin A; D000091345:Protein Glutamine gamma Glutamyltransferase 2; D011503:Transglutaminases; D019204:GTP-Binding Proteins