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001-es BibID:	BIBFORM072048
Első szerző:	Borrelli, M.
Cím:	Intestinal anti-transglutaminase 2 immunoglobulin A deposits in children at risk for coeliac disease (CD) : data from the PreventCD study / Borrelli M., Maglio M., Korponay-Szabó I. R., Vass V., Mearin M. L., Meijer C., Niv-Drori H., Ribes-Koninckx C., Roca M., Shamir R., Troncone R., Auricchio R.
Dátum:	2018
ISSN:	0009-9104
Megjegyzések:	In coeliac disease (CD), anti-tissue transglutaminase 2 immunoglobulin(Ig)A antibodies (anti-TG2) are produced and deposited in the intestine.PreventCD (www.preventcd.com) is a European multi-centre study, whichinvestigates the influence of infant nutrition and that of genetic,immunological and other environmental factors on the risk of developingCD. The aim of the current study was to evaluate the appearance ofintestinal anti-TG2 deposits in very early intestinal biopsies from at-riskinfants and their predictive value for villous atrophy. Sixty-five small bowelbiopsies, performed in 62 children, were investigated for the presenceof intestinal anti-TG2 extracellular IgA deposits by using doubleimmunofluorescence. The biopsies were performed in the presence ofelevated serum levels of CD-associated antibodies and/or symptomssuggesting disease. Deposits of anti-TG2 IgA were present in 53 of 53 CDpatients and three of three potential CD patients. In potential CD patients,mucosal deposits showed a patchy distribution characterized by some areascompletely negative, whereas active CD patients had uniformly present andevident mucosal deposits. Only one of six patients without CD (negative forserum anti-TG2 and with normal mucosa) had intestinal deposits with apatchy distribution and a weak staining. Two of the 53 CD patients receiveda definitive diagnosis of CD after a second or third biopsy; mucosal depositsof anti-TG2 IgA were evaluated in all samples. Before developing villous atrophy, both patients had anti-TG2 deposits in normal mucosalarchitecture, antibodies in one patient being absent in serum. We demonstrated that in CD the intestinal deposits of anti-TG2 are a constant presence and appear very early in the natural history of disease.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban celiac
Megjelenés:	Clinical And Experimental Immunology. - 191 : 3 (2018), p. 311-317. -
További szerzők:	Maglio, M. Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Vass V. Mearin, Maria Luisa Meijer, Caroline R. Niv-Drori, H. Ribes-Koninckx, Carmen Roca, María Shamir, R. Troncone, Riccardo Auricchio, Renata
Pályázati támogatás:	GINOP-2.3.2-15-2016-00015 GINOP NKFI-120392 NKFI OTKA-101788 OTKA
Internet cím:	DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM025025
Első szerző:	Myrsky, Essi
Cím:	Coeliac disease-specific autoantibodies targeted against transglutaminase 2 disturb angiogenesis / Myrsky, E., Kaukinen, K., Syrjänen, M., Korponay-Szabó, I. R., Mäki, M., Lindfors, K.
Dátum:	2008
ISSN:	0009-9104
Megjegyzések:	Coeliac disease is characterized by immunoglobulin-A (IgA)-class autoantibodies targeted against transglutaminase 2 (TG2), a multi-functional protein also with a role in angiogenesis. These antibodies are present in patient serum but are also found bound to TG2 below the epithelial basement membrane and around capillaries in the small intestinal mucosa. Based on these facts and the information that the mucosal vasculature of coeliac patients on a gluten-containing diet is disorganized, we studied whether the coeliac disease-specific autoantibodies targeted against TG2 would disturb angiogenesis. The effects of coeliac disease-specific autoantibodies on in vitro angiogenesis were studied in angiogenic cell cultures. The binding of the antibodies to cells, endothelial sprouting, migration of both endothelial and vascular mesenchymal cells, the integrity of the actin cytoskeleton in both cell types and the differentiation of vascular mesenchymal cells were recorded. In vitro, IgA derived from coeliac disease patients on a gluten-containing diet binds to surface TG2 on endothelial and vascular mesenchymal cells and this binding can be inhibited by the removal of TG2. In addition, coeliac disease-specific autoantibodies targeting TG2 disturb several steps of angiogenesis: endothelial sprouting and the migration of both endothelial and vascular mesenchymal cells. Furthermore, the autoantibodies cause disorganization of the actin cytoskeleton in both capillary cell types that account most probably for the defective cellular migration. We conclude that coeliac disease-specific autoantibodies recognizing TG2 inhibit angiogenesis in vitro. This disturbance of the angiogenic process could lead in vivo to the disruption of the mucosal vasculature seen in coeliac disease patients on a gluten-containing diet.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Clinical And Experimental Immunology. - 152 : 1 (2008), p. 111-119. -
További szerzők:	Kaukinen, Katri Syrjänen, Mari Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Mäki, Markku Lindfors, Katri
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM044272
Első szerző:	Rauhavirta, Tiina
Cím:	Epithelial transport and deamidation of gliadin peptides : a role for coeliac disease patient immunoglobulin A / Rauhavirta, T., Qiao, S.-W., Jiang, Z., Myrsky, E., Loponen, J., Korponay-Szabó, I. R., Salovaara, H., Garcia-Horsman, J. A., Venäläinen, J., Männistö, P. T., Collighan, R., Mongeot, A., Griffin, M., Mäki, M., Kaukinen, K., Lindfors, K.
Dátum:	2011
ISSN:	0009-9104
Megjegyzések:	In coeliac disease, the intake of dietary gluten induces small-bowel mucosal damage and the production of immunoglobulin (Ig)A class autoantibodies against transglutaminase 2 (TG2). We examined the effect of coeliac patient IgA on the apical-to-basal passage of gluten-derived gliadin peptides p31-43 and p57-68 in intestinal epithelial cells. We demonstrate that coeliac IgA enhances the passage of gliadin peptides, which could be abolished by inhibition of TG2 enzymatic activity. Moreover, we also found that both the apical and the basal cell culture media containing the immunogenic gliadin peptides were able to induce the proliferation of deamidation-dependent coeliac patient-derived T cells even in the absence of exogenous TG2. Our results suggest that coeliac patient IgA could play a role in the transepithelial passage of gliadin peptides, a process during which they might be deamidated.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Clinical And Experimental Immunology. - 164 : 1 (2011), p. 127-136. -
További szerzők:	Qiao, Shuo-Wang Jiang, Z. Myrsky, Essi Loponen, J. Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Salovaara, H. Garcia-Horsman, J. Arturo Venäläinen, Jarkko I. Männistö, Pekka T. Collighan, Russell Mongeot, Alexandre Griffin, Martin Mäki, Markku Kaukinen, Katri Lindfors, Katri
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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