%0 Journal Article %J Clin Exp Immunol %D 2016 %T Lack of Evidence of Rotavirus-Dependent Molecular Mimicry as a Trigger of Celiac Disease. %A Ziberna, Fabiana %A De Lorenzo, Giuditta %A Schiavon, Valentina %A Arnoldi, Francesca %A Quaglia, Sara %A De Leo, Luigina %A Vatta, Serena %A Martelossi, Stefano %A Burrone, Oscar R %A Ventura, Alessandro %A Not, Tarcisio %X

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.

%B Clin Exp Immunol %8 2016 Aug 22 %G ENG %1 http://www.ncbi.nlm.nih.gov/pubmed/27548641?dopt=Abstract %R 10.1111/cei.12855