@article {8524,
	title = {Lack of Evidence of Rotavirus-Dependent Molecular Mimicry as a Trigger of Celiac Disease.},
	journal = {Clin Exp Immunol},
	year = {2016},
	month = {2016 Aug 22},
	abstract = {<p>New data suggest the involvement of Rotavirus (RV) in triggering autoimmunity in celiac disease (CD) by molecular mimicry between the human-transglutaminase protein and the dodecapeptide (260-271 aa) of the RV protein VP7 (pVP7). To assess the role of RV in the onset of CD, we measured the anti-pVP7 antibodies in the sera of children with CD and of control groups. We analysed serum samples of 118 biopsy proven CD patients and 46 patients with potential-CD; 32 children with other gastrointestinal diseases; 107 no-CD children and 107 blood donors. By ELISA assay, we measured IgA-IgG antibodies against the synthetic peptides pVP7, the human transglutaminase-derived peptide (476-487 aa) which shows an homology with VP7 protein and a control peptide. The triple-layered RV particles (TLPs), containing the VP7 protein, and the double-layered RV-particles (DLPs), lacking the VP7 protein were also used as antigens in ELISA assay. Antibody reactivity to the RV-TLPs was positive in 22/118 (18\%) CD patients and in both paediatric (17/107, 16\%) and adult (29/107, 27\%) control groups, without showing a statistically significant difference among them (p=0.6, p=0.1). Biopsy-proven CD patients as well as the adult control group demonstrated a high positive antibody reactivity against both pVP7 (34/118, 29\% CD patients; 66/107, 62\% adult controls) and control synthetic peptides (35/118, 30\% CD patients; 56/107, 52\% adult controls) suggesting a non-specific response against RV pVP7. We show that children with CD do not have higher immune reactivity to RV, thus questioning the molecular mimicry mechanism as a triggering factor of CD. This article is protected by copyright. All rights reserved.</p>},
	issn = {1365-2249},
	doi = {10.1111/cei.12855},
	author = {Ziberna, Fabiana and De Lorenzo, Giuditta and Schiavon, Valentina and Arnoldi, Francesca and Quaglia, Sara and De Leo, Luigina and Vatta, Serena and Martelossi, Stefano and Burrone, Oscar R and Ventura, Alessandro and Not, Tarcisio}
}
@article {3617,
	title = {Levels of circulating TNF-related apoptosis-inducing ligand in celiac disease.},
	journal = {Exp Ther Med},
	volume = {8},
	year = {2014},
	month = {2014 Dec},
	pages = {1906-1908},
	abstract = {<p>It has previously been demonstrated that the circulating levels of TNF-related apoptosis-inducing ligand (TRAIL) are significantly lower in patients with type 1 diabetes (T1D) than in normal age- and gender-matched controls. Since celiac disease (CD) is often associated with T1D, a retrospective study was performed to analyze the sera of a cohort of pediatric subjects: i) patients with CD at onset (n=100); ii) patients with potential CD (n=45); iii) patients with CD associated with other auto-immune diseases (n=17); and iv) patients with eosinophilic esophagitis (n=15). Among the patients with CD, 49 were also analyzed after six months on a gluten-free diet, while data were also available for 13 patients after one year on a gluten-free diet. No significant differences were found in the circulating levels of TRAIL between the patients with CD and the patients with either eosinophilic esophagitis or potential CD. Patients with CD associated with other auto-immune diseases showed significantly lower levels of TRAIL when compared with patients with CD alone. The gluten-free diet did not significantly modify the levels of circulating TRAIL at 6 or 12 months. Thus, although T1D and CD share common immunological features, the circulating levels of TRAIL show a significant difference between the two pathologies, and do not appear to be modulated in CD.</p>},
	issn = {1792-0981},
	doi = {10.3892/etm.2014.2026},
	author = {Celeghini, Claudio and Not, Tarcisio and Norcio, Alessia and Monasta, Lorenzo and Secchiero, Paola}
}
