<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">De Leo, Luigina</style></author><author><style face="normal" font="default" size="100%">Aeschlimann, Daniel</style></author><author><style face="normal" font="default" size="100%">Hadjivassiliou, Marios</style></author><author><style face="normal" font="default" size="100%">Aeschlimann, Pascale</style></author><author><style face="normal" font="default" size="100%">Salce, Nicola</style></author><author><style face="normal" font="default" size="100%">Vatta, Serena</style></author><author><style face="normal" font="default" size="100%">Ziberna, Fabiana</style></author><author><style face="normal" font="default" size="100%">Cozzi, Giorgio</style></author><author><style face="normal" font="default" size="100%">Martelossi, Stefano</style></author><author><style face="normal" font="default" size="100%">Ventura, Alessandro</style></author><author><style face="normal" font="default" size="100%">Not, Tarcisio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Anti-transglutaminase 6 Antibody Development in Children With Celiac Disease Correlates With Duration of Gluten Exposure.</style></title><secondary-title><style face="normal" font="default" size="100%">J Pediatr Gastroenterol Nutr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Pediatr. Gastroenterol. Nutr.</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2018</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2018 Jan</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">66</style></volume><pages><style face="normal" font="default" size="100%">64-68</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;OBJECTIVES: &lt;/b&gt;Antibodies against transglutaminase 6 (anti-TG6) have been implicated in neurological manifestations in adult patients with genetic gluten intolerance, and it is unclear whether autoimmunity to TG6 develops following prolonged gluten exposure. We measured the anti-TG6 in children with celiac disease (CD) at the diagnosis time to establish a correlation between these autoantibodies and the duration of gluten exposure. We investigated a correlation between anti-TG6 and the presence of neurological disorders.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;Anti-TG6 (IgA/IgG) were measured by ELISA in sera of children with biopsy-proven CD and of children experiencing gastrointestinal disorders. CD patients positive for anti-TG6 were retested after 2 years of gluten-free diet (GFD).&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;We analyzed the sera of 274 CD children and of 121 controls. Anti-TG6 were detected in 68/274 (25%) CD patients and in 19/121 (16%) controls, with significant difference between the 2 groups (P = 0.04). None of the CD patients and of the controls testing positive for anti-TG6 were experiencing neurological disorders. Eleven of 18 (61%) CD patients with other autoimmune diseases were positive for anti-TG6. In CD patients, a significant correlation between the gluten exposure before the CD diagnosis and anti-TG6 concentration was found (P = 0.006 for IgA; P &lt; 0.0001 for IgG). After GFD anti-TG6 concentrations were significantly reduced (P &lt; 0.001). No significant correlation was observed between anti-TG6 and anti-TG2 serum concentrations.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Anti-TG6 are more prevalent in children with untreated CD in the absence of overt neurological disorders. The synthesis of the anti-TG6 is related to a longer exposure to gluten before the CD diagnosis, and the autoimmunity against TG6 is gluten dependent and disappeared during GFD.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/28542044?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Boscolo, Sabrina</style></author><author><style face="normal" font="default" size="100%">Lorenzon, Andrea</style></author><author><style face="normal" font="default" size="100%">Sblattero, Daniele</style></author><author><style face="normal" font="default" size="100%">Florian, Fiorella</style></author><author><style face="normal" font="default" size="100%">Stebel, Marco</style></author><author><style face="normal" font="default" size="100%">Marzari, Roberto</style></author><author><style face="normal" font="default" size="100%">Not, Tarcisio</style></author><author><style face="normal" font="default" size="100%">Aeschlimann, Daniel</style></author><author><style face="normal" font="default" size="100%">Ventura, Alessandro</style></author><author><style face="normal" font="default" size="100%">Hadjivassiliou, Marios</style></author><author><style face="normal" font="default" size="100%">Tongiorgi, Enrico</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Anti transglutaminase antibodies cause ataxia in mice.</style></title><secondary-title><style face="normal" font="default" size="100%">PLoS One</style></secondary-title><alt-title><style face="normal" font="default" size="100%">PLoS ONE</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Antibodies</style></keyword><keyword><style  face="normal" font="default" size="100%">Ataxia</style></keyword><keyword><style  face="normal" font="default" size="100%">Autoimmune Diseases</style></keyword><keyword><style  face="normal" font="default" size="100%">Brain</style></keyword><keyword><style  face="normal" font="default" size="100%">Celiac Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Gliadin</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Isoenzymes</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice, Inbred C57BL</style></keyword><keyword><style  face="normal" font="default" size="100%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Motor Skills</style></keyword><keyword><style  face="normal" font="default" size="100%">Rats</style></keyword><keyword><style  face="normal" font="default" size="100%">Rats, Sprague-Dawley</style></keyword><keyword><style  face="normal" font="default" size="100%">Transglutaminases</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2010</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2010</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">5</style></volume><pages><style face="normal" font="default" size="100%">e9698</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;BACKGROUND: &lt;/b&gt;Celiac disease (CD) is an autoimmune gastrointestinal disorder characterized by the presence of anti-transglutaminase 2 (TG2) and anti-gliadin antibodies. Amongst the neurological dysfunctions associated with CD, ataxia represents the most common one.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;We analyzed by immunohistochemistry, the anti-neural reactivity of the serum from 20 CD patients. To determine the role of anti-TG2 antibodies in ataxia, two anti-TG2 single chain variable fragments (scFv), isolated from a phage-display IgA antibody library, were characterized by immunohistochemistry and ELISA, and injected in mice to study their effects on motor coordination. We found that 75% of the CD patient population without evidence of neurological involvement, has circulating anti-neural IgA and/or IgG antibodies. Two anti-TG2 scFvs, cloned from one CD patient, stained blood vessels but only one reacted with neurons. This anti-TG2 antibody showed cross reactivity with the transglutaminase isozymes TG3 and TG6. Intraventricular injection of the anti-TG2 or the anti-TG2/3/6 cross-reactive scFv provoked transient, equally intensive ataxia in mice.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;The serum from CD patients contains anti-TG2, TG3 and TG6 antibodies that may potentially cause ataxia.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">3</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/20300628?dopt=Abstract</style></custom1></record></records></xml>