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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
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM044274
Első szerző:	Martucciello, Stefania
Cím:	RhoB is associated with the anti-angiogenic effects of celiac patient transglutaminase 2-targeted autoantibodies / Martucciello Stefania, Lavric Miha, Toth Boglarka, Korponay-Szabo Ilma, Nadalutti Cristina, Myrsky Essi, Rauhavirta Tiina, Esposito Carla, Sulic Ana-Marija, Sblattero Daniele, Marzari Roberto, Mäki Markku, Kaukinen Katri, Lindfors Katri, Caja Sergio
Dátum:	2012
ISSN:	0946-2716
Megjegyzések:	Celiac patient-derived anti-transglutaminase 2 (TG2) antibodies disturb several steps in angiogenesis, but the detailed molecular basis is not known. Therefore, we here analyzed by microarray technology the expression of a set of genes related to angiogenesis and endothelial cell biology in order to identify factors that could explain our previous data related to vascular biology in the context of celiac disease. To this end, in vitro models using human umbilical vein endothelial cells (HUVECs) or in vivo models of angiogenesis were used. A total of 116 genes were analyzed after treatment with celiac patient autoantibodies against TG2. Compared to treatment with control IgA celiac patient, total IgA induced a consistent expression change of 10 genes, the up-regulation of four and down-regulation of six. Of these genes the up-regulated RhoB was selected for further studies. RhoB expression was found to be up-regulated at both messenger RNA and protein level in response to celiac patient total IgA as well as anti-TG2-specific antibody derived from a celiac patient. Interestingly, down-regulation of RhoB by specific small interfering RNA treatment in endothelial cells could rescue the deranged endothelial length and tubule formation caused by celiac disease autoantibodies. RhoB function is controlled by its post-translational modification by farnesylation. This modification of RhoB required for its correct function can be prevented by the cholesterol lowering drug simvastatin, which was also able to abolish the anti-angiogenic effects of celiac anti-TG2 autoantibodies. Taken together, our results would suggest that RhoB plays a key role in the response of endothelial cells to celiac disease-specific anti-TG2 autoantibodies
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Journal Of Molecular Medicine-Jmm. - 90 : 7 (2012), p. 817-826. -
További szerzők:	Lavric, Miha Tóth Boglárka Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Nadalutti, Cristina Myrsky, Essi Rauhavirta, Tiina Esposito, Carla Sulic, Ana-Marija Sblattero, Daniele Marzari, Roberto Mäki, Markku Kaukinen, Katri Lindfors, Katri Caja, Sergio
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