@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 {7776,
	title = {Legius syndrome: case report and review of literature.},
	journal = {Ital J Pediatr},
	volume = {41},
	year = {2015},
	month = {2015},
	pages = {8},
	abstract = {<p>A 8-month-old child was referred to our Dermatologic Unit for suspected Neurofibromatosis type 1 (NF 1), because of the appearance, since few days after birth, of numerous caf{\'e}-au-lait spots (seven larger than 5 mm); no other sign evocative of NF 1 was found. Her family history was remarkable for the presence of multiple caf{\'e}-au-lait spots in the mother, the grandfather and two aunts. The family had been already examined for NF 1, but no sign evocative of the disease was found. We then suspected Legius syndrome, a dominant disease characterized by a mild neurofibromatosis 1 phenotype. The diagnosis was confirmed by the finding of a mutation in SPRED1 gene, a feedback regulator of RAS/MAPK signaling. Here, we discuss the differential diagnosis of caf{\`e}-au-lait spots and we briefly review the existing literature about Legius syndrome.</p>},
	issn = {1824-7288},
	doi = {10.1186/s13052-015-0115-9},
	author = {Benelli, Elisa and Bruno, Irene and Belcaro, Chiara and Ventura, Alessandro and Berti, Irene}
}
