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1.

001-es BibID:BIBFORM048561
Első szerző:Antonella Nadalutti, Cristina
Cím:Thioredoxin Is Involved in Endothelial Cell Extracellular Transglutaminase 2 Activation Mediated by Celiac Disease Patient IgA / Cristina Antonella Nadalutti, Ilma Rita Korponay-Szabo, Katri Kaukinen, Zhuo Wang, Martin Griffin, Markku Mäki, Katri Lindfors
Dátum:2013
ISSN:1932-6203
Megjegyzések:PURPOSE:To investigate the role of thioredoxin (TRX), a novel regulator of extracellular transglutaminase 2 (TG2), in celiac patients IgA (CD IgA) mediated TG2 enzymatic activation.METHODS:TG2 enzymatic activity was evaluated in endothelial cells (HUVECs) under different experimental conditions by ELISA and Western blotting. Extracellular TG2 expression was studied by ELISA and immunofluorescence. TRX was analysed by Western blotting and ELISA. Serum immunoglobulins class A from healthy subjects (H IgA) were used as controls. Extracellular TG2 enzymatic activity was inhibited by R281. PX12, a TRX inhibitor, was also employed in the present study.RESULTS:We have found that in HUVECs CD IgA is able to induce the activation of extracellular TG2 in a dose-dependent manner. Particularly, we noted that the extracellular modulation of TG2 activity mediated by CD IgA occurred only under reducing conditions, also needed to maintain antibody binding. Furthermore, CD IgA-treated HUVECs were characterized by a slightly augmented TG2 surface expression which was independent from extracellular TG2 activation. We also observed that HUVECs cultured in the presence of CD IgA evinced decreased TRX surface expression, coupled with increased secretion of the protein into the culture medium. Intriguingly, inhibition of TRX after CD IgA treatment was able to overcome most of the CD IgA-mediated effects including the TG2 extracellular transamidase activity.CONCLUSIONS:Altogether our findings suggest that in endothelial cells CD IgA mediate the constitutive activation of extracellular TG2 by a mechanism involving the redox sensor protein TRX.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Thioredoxin
IgA
TG2
Megjelenés:Plos One. - 8 : 10 (2013), p. e77277. -
További szerzők:Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Kaukinen, Katri Wang, Zhuo Griffin, Martin Mäki, Markku Lindfors, Katri
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2.

001-es BibID:BIBFORM011928
Első szerző:Caja, Sergio
Cím:Inhibition of transglutaminase 2 enzymatic activity ameliorates the anti-angiogenic effects of coeliac disease autoantibodies / Caja S., Myrsky E., Korponay-Szabo I., Nadalutti C., Sulic A. M., Lavric M., Sblattero D., Marzari R., Collighan R., Mongeot A., Griffin M., Maki M., Kaukinen K., Lindfors K.
Dátum:2010
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Scandinavian Journal of Gastroenterology. - 45 : 4 (2010), p. 421-427. -
További szerzők:Myrsky, Essi Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Nadalutti, Cristina Sulic, Ana-Marija Lavric, Miha Sblattero, Daniele Marzari, Roberto Collighan, Russell Mongeot, Alexandre Griffin, Martin Mäki, Markku Kaukinen, Katri Lindfors, Katri
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3.

001-es BibID:BIBFORM044302
Első szerző:Collin, Pekka
Cím:Antiendomysial and antihuman recombinant tissue transglutaminase antibodies in the diagnosis of coeliac disease : a biopsy-proven European multicentre study / Collin Pekka, Kaukinen Katri, Vogelsang Harald, Korponay-Szabo Ilma, Sommer Rudolf, Schreier Elisabeth, Volta Umberto, Granito Alessandro, Veronesi Lorenza, Mascart Francoise, Ocmant Annick, Ivarsson Anneli, Lagerqvist Carina, Bürgin-Wolff Annemarie, Hadziselimovic Faruk, Furlano Raoul I., Sidler Marc A., Mulder Chris J. J., Goerres Marije S., Mearin M. Luisa, Ninaber Maarten K., Gudmand-Hoyer Eivind, Fabiani Elisabetta, Catassi Carlo, Tidlund Helena, Alainentalo Lisbeth, Maki Markku
Dátum:2005
ISSN:0954-691X
Megjegyzések:OBJECTIVE:To investigate the value of serum antitissue transglutaminase IgA antibodies (IgA-TTG) and IgA antiendomysial antibodies (IgA-EMA) in the diagnosis of coeliac disease in cohorts from different geographical areas in Europe. The setting allowed a further comparison between the antibody results and the conventional small-intestinal histology.METHODS:A total of 144 cases with coeliac disease [median age 19.5 years (range 0.9-81.4)], and 127 disease controls [median age 29.2 years (range 0.5-79.0)], were recruited, on the basis of biopsy, from 13 centres in nine countries. All biopsy specimens were re-evaluated and classified blindly a second time by two investigators. IgA-TTG were determined by ELISA with human recombinant antigen and IgA-EMA by an immunofluorescence test with human umbilical cord as antigen.RESULTS:The quality of the biopsy specimens was not acceptable in 29 (10.7%) of 271 cases and a reliable judgement could not be made, mainly due to poor orientation of the samples. The primary clinical diagnosis and the second classification of the biopsy specimens were divergent in nine cases, and one patient was initially enrolled in the wrong group. Thus, 126 coeliac patients and 106 controls, verified by biopsy, remained for final analysis. The sensitivity of IgA-TTG was 94% and IgA-EMA 89%, the specificity was 99% and 98%, respectively.CONCLUSIONS:Serum IgA-TTG measurement is effective and at least as good as IgA-EMA in the identification of coeliac disease. Due to a high percentage of poor histological specimens, the diagnosis of coeliac disease should not depend only on biopsy, but in addition the clinical picture and serology should be considered
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:European Journal Of Gastroenterology & Hepatology. - 17 : 1 (2005), p. 85-91. -
További szerzők:Kaukinen, Katri Vogelsang, Harald Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Sommer, Rudolf Schreier, Elisabeth Volta, Umberto Granito, Alessandro Veronesi, Lorenza Mascart, Francoise Ocmant, Annick Ivarsson, Anneli Lagerqvist, Carina Bürgin-Wolff, Annemarie Hadziselimovic, Faruk Furlano, Raoul I. Sidler, Marc A. Mulder, Chris J. Goerres, Marije S. Mearin, Maria Luisa Ninaber, Maarten K. Gudmand-Hoyer, Eivind Fabiani, Elisabetta Catassi, Carlo Tidlund, Helena Alainentalo, Lisbeth Mäki, Markku
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4.

001-es BibID:BIBFORM016242
Első szerző:Dubois, Patrick C. A.
Cím:Multiple common variants for celiac disease influencing immune gene expression / Dubois Patrick C. A., Trynka Gosia, Franke Lude, Hunt Karen A., Romanos Jihane, Curtotti Alessandra, Zhernakova Alexandra, Heap Graham A. R., Ádány Róza, Aromaa Arpo, Bardella Maria Teresa, van den Berg Leonard H., Bockett Nicholas A., de la Concha Emilio G., Dema Bárbara, Fehrmann Rudolf S. N., Fernández-Arquero Miguel, Fiatal Szilvia, Grandone Elvira, Green Peter M., Groen Harry J. M., Gwilliam Rhian, Houwen Roderick H. J., Hunt Sarah E., Kaukinen Katri, Kelleher Dermot, Korponay-Szabo Ilma, Kurppa Kalle, MacMathuna Padraic, Mäki Markku, Mazzilli Maria Cristina, McCann Owen T., Mearin M. Luisa, Mein Charles A., Mirza Muddassar M., Mistry Vanisha, Mora Barbara, Morley Katherine I., Mulder Chris J., Murray Joseph A., Núnez Concepción, Oosterom Elvira, Ophoff Roel A., Polanco Isabel, Peltonen Leena, Platteel Mathieu, Rybak Anna, Salomaa Veikko, Schweizer Joachim J., Sperandeo Maria Pia, Tack Greetje J., Turner Graham, Veldink Jan H., Verbeek Wieke H. M., Weersma Rinse K., Wolters Victorien M., Urcelay Elena, Cukrowska Bozena, Greco Luigi, Neuhausen Susan L., McManus Ross, Barisani Donatella, Deloukas Panos, Barrett Jeffrey C., Saavalainen Paivi, Wijmenga Cisca, van Heel David A.
Dátum:2010
ISSN:1061-4036
Tárgyszavak:Orvostudományok Egészségtudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Nature Genetics. - 42 : 4 (2010), p. 295-302. -
További szerzők:Trynka, Gosia Franke, Lude Hunt, Karen A. Romanos, Jihane Curtotti, Alessandra Zhernakova, Alexandra Heap, Graham A. R. Ádány Róza (1952-) (megelőző orvostan és népegészségtan szakorvos) Aromaa, Arpo Bardella, Maria Teresa Van den Berg, Leonard H. Bockett, Nicholas A. Concha, Emilio G., de la Dema, Bárbara Fehrmann, Rudolf S. N. Fernández-Arquero, Miguel Fiatal Szilvia (1978-) (epidemiológus, népegészségügyi szakember) Grandone, Elvira Green, Peter M. Groen, Harry J. M. Gwilliam, Rhian Houwen, Roderick H. J. Hunt, Sarah E. Kaukinen, Katri Kelleher, Dermot Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Kurppa, Kalle MacMathuna, Padraic Mäki, Markku Mazzilli, Maria Cristina McCann, Owen T. Mearin, Maria Luisa Mein, Charles A. Mirza, Muddassar M. Mistry, Vanisha Mora, Barbara Morley, Katherine I. Mulder, Chris J. Murray, Joseph A. Núnez, Concepción Oosterom, Elvira Ophoff, Roel A. Polanco, Isabel Peltonen, Leena Platteel, Mathieu Rybak, Anna Salomaa, Veikko Schweizer, Joachim J. Sperandeo, Maria Pia Tack, Greetje J. Turner, Graham Veldink, Jan H. Verbeek, Wieke H. M. Weersma, Rinse K. Wolters, Victorien M. Urcelay, Elena Cukrowska, Bozena Greco, Luigi Neuhausen, Susan L. McManus, Ross Barisani, Donatella Deloukas, Panos Barrett, Jeffrey C. Saavalainen, Päivi Wijmenga, Cisca Heel, David A., van
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5.

001-es BibID:BIBFORM044276
Első szerző:Einarsdottir, Elisabet
Cím:Multiple independent variants in 6q21-22 associated with susceptibility to celiac disease in the Dutch, Finnish and Hungarian populations / Einarsdottir Elisabet, Bevova Marianna R., Zhernakova Alexandra, Monsuur Alienke, Koskinen Lotta L. E., van't Slot Ruben, Mulder Chris, Mearin M. Luisa, Korponay-Szabo Ilma R., Kaukinen Katri, Kurppa Kalle, Kere Juha, Mäki Markku, Wijmenga Cisca, Saavalainen Päivi
Dátum:2011
ISSN:1018-4813
Megjegyzések:Celiac disease is an inflammatory enteropathy caused by intolerance to gluten. Previous linkage studies in the Dutch, Finnish and Hungarian populations have revealed a locus on chromosome 6q21-22 conferring susceptibility to celiac disease. This locus has previously been implicated in susceptibility to other autoimmune diseases such as Crohn's disease and type 1 diabetes. We performed fine mapping on 446 independent individuals with celiac disease and 641 controls of Dutch origin, testing 872 tagging SNPs in a 22 Mb region of chromosome 6. The 12 most promising SNPs were followed up in 2071 individuals from 284 Finnish and 357 Hungarian celiac disease families to identify risk variants in this region. Multiple markers in the region were significantly associated with celiac disease in the Dutch material. Two SNPs, rs9391227 and rs4946111, were significantly associated with celiac disease in the Finnish population. The association to rs9391227 represents the strongest association signal found in the Finnish (P = 0.003, OR 0.66) as well as the combined Dutch, Finnish and Hungarian populations (P = 3.6 ? 10(-5), OR 0.76). The rs9391227 is situated downstream of the HECT domain and ankyrin repeat containing, E3 ubiquitin protein ligase 1 (HACE1) gene and is contained within a region of strong linkage disequilibrium enclosing HACE1. Two additional, independent, susceptibility variants in the 6q21-22 region were also found in a meta-analysis of the three populations. The 6q21-22 region was confirmed as a celiac disease susceptibility locus and harbors multiple independent associations, some of which may implicate ubiquitin-pathways in celiac disease susceptibility.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:European Journal Of Human Genetics. - 19 : 6 (2011), p. 682-686. -
További szerzők:Bevova, Marianna R. Zhernakova, Alexandra Monsuur, Alienke Koskinen, Lotta L. E. van't Slot, Ruben Mulder, Chris J. Mearin, Maria Luisa Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Kaukinen, Katri Kurppa, Kalle Kere, Juha Mäki, Markku Wijmenga, Cisca Saavalainen, Päivi
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6.

001-es BibID:BIBFORM037276
Első szerző:Einarsdottir, Elisabet
Cím:Genome-wide analysis of extended pedigrees confirms IL2-IL21 linkage and shows additional regions of interest potentially influencing coeliac disease risk / Einarsdottir, E., Koskinen, L. L. E., de Kauwe, A. L., Dukes, E., Mustalahti, K., Balogh, M., Korponay-Szabo, I. R., Kaukinen, K., Kurppa, K., Ádány, R., Pocsai, Z., Széles, G., Mäki, M., Kere, J., Saavalainen, P.
Dátum:2011
ISSN:0001-2815
Megjegyzések:Coeliac disease is a chronic inflammatory condition of the small intestine, triggered by dietary exposure to gluten in genetically susceptible individuals. Risk alleles at HLA-DQA1 and HLA-DQB1 are necessary for disease development, but are alone not sufficient for disease onset. We aimed to identify novel loci underlying susceptibility to coeliac disease through the use of extended Finnish and Hungarian families with multiple affected individuals. An initial whole-genome linkage approach yielded several loci that were followed up further using the Immunochip custom array. Loci with a parametric logarithm of odds (LOD) score of >1.3 were identified at 4q, 6p [human leukocyte antigen (HLA) region], 6q, 7p, 17p, 17q and at 22p. The 4q and 6q loci have been identified previously in coeliac disease risk, whereas follow-up analyses indicate that the 17p and 22p loci may be novel risk loci for coeliac disease. These loci harbour previously described risk variants for other autoimmune diseases, but their segregation patterns do not explain the linkage to coeliac disease. We followed up the linkage to the 4q region, containing the previously described interleukin (IL)2 and IL21 genes. The risk variants at 4q in the studied pedigrees are most likely distinct from previously described risk variants, indicating that the observed linkage may be due to rare high-risk variants of still unknown nature. The importance of this locus to coeliac disease risk was further shown by the finding that serum levels of IL21 were elevated in both untreated and treated coeliac patients compared to controls.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Tissue Antigens. - 78 : 6 (2011), p. 428-437. -
További szerzők:Koskinen, Lotta L. E. de Kauwe, A. Dukes, Emma Mustalahti, Kirsi Balogh M. Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Kaukinen, Katri Kurppa, Kalle Ádány Róza (1952-) (megelőző orvostan és népegészségtan szakorvos) Pocsai Zsuzsanna (1970-) (népegészségügyi szakember) Széles György (1969-) (epidemiológus) Mäki, Markku Kere, Juha Saavalainen, Päivi
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7.

001-es BibID:BIBFORM009647
Első szerző:Einarsdottir, Elisabet
Cím:IL23R in the Swedish, Finnish, Hungarian and Italian populations : association with IBD and psoriasis, and linkage to celiac disease / Elisabet Einarsdottir, Lotta L. E. Koskinen, Emma Dukes, Kati Kainu, Sari Suomela, Marit Lappalainen, Fabiana Ziberna, Korponay-Szabó Ilma, Kalle Kurppa, Katri Kaukinen, Ádány Róza, Pocsai Zsuzsa, Széles György, Martti Farkkila, Ulla Turunen, Leena Halme, Paulina Paavola-Sakki, Tarcisio Not, Serena Vatta, Alessandro Ventura, Robert Löfberg, Leif Torkvist, Francesca Bresso, Jonas Halfvarson, Markku Maki, Kimmo Kontula, Ulpu Saarialho-Kere, Juha Kere, Mauro D'Amato, Päivi Saavalainen
Dátum:2009
Tárgyszavak:Orvostudományok Egészségtudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:BMC Medical Genetics [electronic resource]. - 10 : 8 (2009), p. 1-10. -
További szerzők:Koskinen, Lotta L. E. Dukes, Emma Kainu, Kati Suomela, Sari Lappalainen, Marit Ziberna, Fabiana Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Kurppa, Kalle Kaukinen, Katri Ádány Róza (1952-) (megelőző orvostan és népegészségtan szakorvos) Pocsai Zsuzsanna (1970-) (népegészségügyi szakember) Széles György (1969-) (epidemiológus) Farkkila, Martti Turunen, Ulla Halme, Leena Paavola-Sakki, Paulina Not, Tarcisio Vatta, Serena Ventura, Alessandro Löfberg, Robert Torkvist, Leif Bresso, Francesca Halfvarson, Jonas Mäki, Markku Kontula, Kimmo Saarialho-Kere, Ulpu Kere, Juha D'Amato, Mauro Saavalainen, Päivi
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8.

001-es BibID:BIBFORM002290
Első szerző:Garcia-Horsman, J. Arturo
Cím:Deficient activity of mammalian prolyl oligopeptidase on the immunoactive peptide digestion in coeliac disease / J. Arturo Garcia-Horsman, Jarkko I. Venäläinen, Olli Lohi, I. Seppo Auriola, Ilma R. Korponay-Szabó, Katri Kaukinen, Markku Mäki, Pekka T. Männistö
Dátum:2007
Megjegyzések:Objective. Gliadin digestion-resistant peptides are harmful in coeliac disease (CD), and initiate an autoimmune reaction that cause a cascade of symptoms. The role of the endogenous prolyl oligopeptidase (POP) is still not clear, and its activity over gliadin immunoactive peptides has not been fully established. Our objective was therefore to determine the endogenous POP protein level, tissue distribution and total activity in normal and CD epithelia, to evaluate tissue peptidase activity over gliadin peptides, and compare this with activities of mammalian POP and rat intestinal extracts. Material and methods. POP was assayed in biopsy preparations enzymatically and by Western blot analysis. Distribution was studied by immunohistochemistry using a specific POP antibody. Peptide cleavage was followed by mass spectroscopy-highperformance liquid chromatography (MS-HPLC). Results. There was no difference in POP activity between normal and CD samples, but those from active CD subjects had an even higher ability to degrade the 33-mer peptide than those from treated CD and healthy humans. POP locates intracellularly in epithelia, similarly to dipeptidyl peptidase IV (DPPIV), but the latter is clearly found in normal microvilli but less so in diseased microvilli. Mammalian POP is unable to digest 33-mer peptide, which, conversely, is a POP inhibitor. Rat intestine is more effective than human intestine in cleaving the 33-mer peptide. However, the products are still harmful epitopes. A surplus of POP eliminates 12-mer and 19-mer peptide products. Conclusions. The results rule out a causative role of POP in the pathogenesis of CD and strongly suggest that other peptidases are needed to eliminate gliadin-derived, immunoactive and toxic peptides larger than 33-mer, which is a POP inhibitor.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
coeliac disease
digestion
gliadin
peptidase
prolyl oligopeptidase
Megjelenés:Scandinavian Journal of Gastroenterology 42 : 5 (2007), p. 562-571. -
További szerzők:Venäläinen, Jarkko I. Lohi, Olli Auriola, I. Seppo Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Kaukinen, Katri Mäki, Markku Männistö, Pekka T.
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9.

001-es BibID:BIBFORM006244
Első szerző:Haimila, Katri
Cím:The shared CTLA4-ICOS risk locus in celiac disease, IgA deficiency and common variable immunodeficiency / K. Haimila, E. Einarsdottir, A. de Kauwe, L. L. Koskinen, Q. Pan-Hammarström, T. Kaartinen, K. Kurppa, F. Ziberna, T. Not, S. Vatta, A. Ventura, I. R. Korponay-Szabó, R. Ádány, Z. Pocsai, G. Széles, E. Dukes, K. Kaukinen, M. Mäki, S. Koskinen, J. Partanen, L. Hammarström, P. Saavalainen
Dátum:2009
Tárgyszavak:Orvostudományok Egészségtudományok idegen nyelvű folyóiratközlemény külföldi lapban
IgAD
genetic linkage
association
celia disease
Megjelenés:Genes and Immunity 10 : 2 (2009), p. 151-161. -
További szerzők:Einarsdottir, Elisabet de Kauwe, A. Koskinen, Lotta L. E. Pan-Hammarström, Qiang Kaartinen, Tanja Kurppa, Kalle Ziberna, Fabiana Not, Tarcisio Vatta, Serena Ventura, Alessandro Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Ádány Róza (1952-) (megelőző orvostan és népegészségtan szakorvos) Pocsai Zsuzsanna (1970-) (népegészségügyi szakember) Széles György (1969-) (epidemiológus) Dukes, Emma Kaukinen, Katri Mäki, Markku Koskinen, Seppo Partanen, Jukka Hammarström, Lennart Saavalainen, Päivi
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10.

001-es BibID:BIBFORM069472
Első szerző:Kalliokoski, Suvi
Cím:Transglutaminase 2-specific coeliac disease autoantibodies induce morphological changes and signs of inflammation in the small-bowel mucosa of mice / Suvi Kalliokoski, Victoria Ortín Piqueras, Rafael Frías, Ana-Marija Sulic, Juha A. E. Määttä, Niklas Kähkönen, Keijo Viiri, Heini Huhtala, Arja Pasternack, Kaija Laurila, Daniele Sblattero, Ilma R. Korponay-Szabó, Markku Mäki, Sergio Caja, Katri Kaukinen, Katri Lindfors
Dátum:2017
ISSN:0939-4451 1438-2199
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Amino Acids 49 : 3 (2017), p. 529-540. -
További szerzők:Piqueras, Victoria Ortín Frías, Rafael Sulic, Ana-Marija Määttä, Juha A. E. Kähkönen, Niklas Viiri, Keijo Huhtala, Heini Pasternack, Arja Laurila, Kaija Sblattero, Daniele Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Mäki, Markku Caja, Sergio Kaukinen, Katri Lindfors, Katri
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11.

001-es BibID:BIBFORM056541
Első szerző:Kalliokoski, Suvi
Cím:Injection of celiac disease patient sera or immunoglobulins to mice reproduces a condition mimicking early developing celiac disease / Suvi Kalliokoski, Sergio Caja, Rafael Frias, Kaija Laurila, Outi Koskinen, Onni Niemelä, Markku Mäki, Katri Kaukinen, Ilma R. Korponay-Szabó, Katri Lindfors
Dátum:2015
ISSN:0946-2716
Megjegyzések:Typical features of celiac disease are small-bowel villus atrophy, crypt hyperplasia, and inflammation which develop gradually concomitant with ingestion of gluten. In addition, patients have anti-transglutaminase 2 (TG2) autoantibodies in their serum and tissues. The aim of this study was to establish whether celiac disease can be passively transferred to mice by serum or immunoglobulins. Serum aliquots or purified immunoglobulins (Ig) were intraperitoneally injected into Hsd:Athymic Nude-Foxn1nu mice for 8 or 27 days. As mice do not have proper IgA transport from peritoneum to blood, sera with a high content of IgG class anti-TG2 antibodies from untreated IgA-deficient celiac patients were used. Mouse sera were tested for celiac disease-specific autoantibodies, and several tissues were analyzed for autoantibody deposits targeted to TG2. Morphological assessment was made of the murine small intestinal mucosa. Injection of celiac disease patient sera or total IgG led to a significant delay in weight gain and mild diarrhea in a subset of mice. The mice injected with celiac patient sera or IgG had significantly decreased villus height crypt depth (Vh/CrD) ratios and celiac diseasespecific autoantibody deposits targeted to TG2 in several tissues, including the small intestine. None of these features were observed in control mice. We conclude that administration of IgA-deficient celiac disease patient serum or total IgG induces both deterioration of the intestinal mucosa and clinical features of celiac disease in mice. The experimentally induced condition in the mice injected with patient serum or IgG resembles early developing celiac disease in humans.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Autoantibodies
Celiac disease
Passivetransfer
Transglutaminase 2
Megjelenés:Journal of Molecular Medicine-Jmm 93 : 1 (2015), p. 51-62. -
További szerzők:Caja, Sergio Frías, Rafael Laurila, Kaija Koskinen, Outi Niemelä, Onni Mäki, Markku Kaukinen, Katri Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Lindfors, Katri
Pályázati támogatás:101788
OTKA
TÁMOP-4.2.2.A-11/1/KONV-2012-0023
TÁMOP
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12.

001-es BibID:BIBFORM048568
035-os BibID:Article ID: e65887
Első szerző:Kalliokoski, Suvi
Cím:Celiac Disease-Specific TG2-Targeted Autoantibodies Inhibit Angiogenesis Ex Vivo and In Vivo in Mice by Interfering with Endothelial Cell Dynamics / Suvi Kalliokoski, Ana-Marija Sulic, Ilma R. Korponay-Szabo, Zsuzsa Szondy, Rafael Frias, Mileidys Alea Perez, Stefania Martucciello, Anne Roivainen, Lauri J. Pelliniemi, Carla Esposito, Martin Griffin, Daniele Sblattero, Markku Mäki, Katri Kaukinen, Katri Lindfors, Sergio Caja
Dátum:2013
ISSN:1932-6203
Megjegyzések:A characteristic feature of celiac disease is the presence of circulating autoantibodies targeted against transglutaminase 2 (TG2), reputed to have a function in angiogenesis. In this study we investigated whether TG2-specific autoantibodies derived from celiac patients inhibit angiogenesis in both ex vivo and in vivo models and sought to clarify the mechanism behind this phenomenon. We used the ex vivo murine aorta-ring and the in vivo mouse matrigel-plug assays to address aforementioned issues. We found angiogenesis to be impaired as a result of celiac disease antibody supplementation in both systems. Our results also showed the dynamics of endothelial cells was affected in the presence of celiac antibodies. In the in vivo angiogenesis assays, the vessels formed were able to transport blood despite impairment of functionality after treatment with celiac autoantibodies, as revealed by positron emission tomography. We conclude that celiac autoantibodies inhibit angiogenesis ex vivo and in vivo and impair vascular functionality. Our data suggest that the anti-angiogenic mechanism of the celiac disease-specific autoantibodies involves extracellular TG2 and inhibited endothelial cell mobility.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Plos One [electronic resource]. - 8 : 6 (2013), [8] p. -
További szerzők:Sulic, Ana-Marija Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Szondy Zsuzsanna (1959-) (molekuláris sejtbiológus, biokémikus) Frías, Rafael Perez, Mileidys Alea Martucciello, Stefania Roivainen, Anne Pelliniemi, Lauri J. Esposito, Carla Griffin, Martin Sblattero, Daniele Mäki, Markku Kaukinen, Katri Lindfors, Katri Caja, Sergio
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