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001-es BibID:BIBFORM042703
035-os BibID:PMID:15082580
Első szerző:Korponay-Szabó Ilma (gyermekgyógyász)
Cím:In vivo targeting of intestinal and extraintestinal transglutaminase 2 by coeliac autoantibodies / I. R. Korponay-Szabo, T. Halttunen, Z. Szalai, K. Laurila, R. Király, J. B. Kovács, L. Fésüs, M. Mäki
Dátum:2004
ISSN:0017-5749
Megjegyzések:BACKGROUND: IgA class serum autoantibodies against type 2 (tissue) transglutaminase (TG2) bind to both intestinal and extraintestinal normal tissue sections in vitro, eliciting endomysial, reticulin, and jejunal antibody reactions. It is not known whether similar binding also occurs in coeliac patients in vivo, and may thereby contribute to disease manifestations. AIMS: To investigate intestinal and extraintestinal coeliac tissues for the presence of in vivo bound TG2 specific IgA and its relation to small intestinal mucosal atrophy. PATIENTS: We investigated jejunal samples with normal villous morphology from 10 patients with developing coeliac disease who subsequently progressed to a flat lesion, from 11 patients with dermatitis herpetiformis, and from 12 non-coeliac controls. Six extrajejunal biopsy samples (liver, lymph node, muscle, appendix), obtained based on independent clinical indications from patients with active coeliac disease, were also studied. METHODS: Double colour immunofluorescent studies for in situ IgA, TG2, and laminin were performed. IgA was eluted from tissue sections and tested for TG2 specificity by enzyme linked immunosorbent assay and indirect immunofluorescence. RESULTS: IgA (in one IgA deficient case IgG) deposition on extracellularly located TG2 was detected in jejunal and extrajejunal specimens of all coeliac patients, and also in seven of 11 dermatitis herpetiformis patients, of whom two had no circulating endomysial antibodies. IgA eluted from extraintestinal coeliac tissues was targeted against TG2. CONCLUSIONS: Coeliac IgA targets jejunal TG2 early in disease development even when endomysial antibodies are not present in the circulation. Extraintestinal target sites of coeliac IgA further indicate that humoral immunity may have a pathogenetic role.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Gut. - 53 : 5 (2004), p. 641-648. -
További szerzők:Halttunen, Tuula Szalai Zoltán Laurila, Kaija Király Róbert (1975-) (biológus) Kovács J. Béla Fésüs László (1947-) (orvos biokémikus) Mäki, Markku
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001-es BibID:BIBFORM028773
Első szerző:Korponay-Szabó Ilma (gyermekgyógyász)
Cím:Missing endomysial and reticulin binding of coeliac antibodies in transglutaminase 2 knockout tissues / I. R. Korponay-Szabó, K. Laurila, Zs. Szondy, T. Halttunen, Z. Szalai, I. Dahlbom, I. Rantala, J. B. Kovács, L. Fésüs, M. Mäki
Dátum:2003
ISSN:0017-5749
Megjegyzések:Autoantibodies against transglutaminase 2 (TG2) are thought to be responsible for the endomysial (EMA), reticulin (ARA), and jejunal antibody (JEA) tissue binding of serum samples from coeliac patients but the exclusive role of TG2 in these staining patterns has not yet been established. AIMS: To evaluate whether antigens other than TG2 contribute to EMA/ARA/JEA reactions. PATIENTS: Serum samples from 61 EMA/ARA/JEA positive untreated patients with coeliac disease, 40 dermatitis herpetiformis patients, and 34 EMA/ARA/JEA negative non-coeliac controls were tested. METHODS: TG2 knockout (TG2-/-) and wild-type mouse oesophagus, jejunum, liver, and kidney sections, and TG2-/- sections coated with human recombinant TG2 were used as substrates in single and double immunofluorescent studies for patient IgA binding and tissue localisation of TG2, fibronectin, actin, and calreticulin. RESULTS: None of the patient serum samples elicited EMA, ARA, or JEA binding in TG2-/- morphologically normal tissues. In contrast, 96 of 101 gluten sensitive patient samples (95%) reacted with wild-type mouse tissues and all 101 reacted in EMA/ARA/JEA patterns with TG2-/- mouse tissues coated with human TG2. Serum IgA binding to TG2-/- smooth muscle cells was observed in low titres in 31.1%, 27.5%, and 20.5%, and to TG2-/- epithelium in 26.3%, 5.0%, and 8.8% of coeliac, dermatitis herpetiformis, and control samples, respectively. These positivities partly colocalised with actin and calreticulin but not with TG2 or fibronectin. CONCLUSIONS: EMA/ARA/JEA antibody binding patterns are exclusively TG2 dependent both in coeliac and dermatitis herpetiformis patients. Actin antibodies are responsible for some positivities which are not part of the EMA/ARA/JEA reactions.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Gut 52 : 2 (2003), p. 199-204. -
További szerzők:Laurila, Kaija Szondy Zsuzsanna (1959-) (molekuláris sejtbiológus, biokémikus) Halttunen, Tuula Szalai Zoltán Dahlbom, Ingrid Rantala, I. Kovács B. J. Fésüs László (1947-) (orvos biokémikus) Mäki, Markku
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
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