Gluten ataxia: passive transfer in a mouse model.
Gluten sensitivity is an autoimmune disease that usually causes intestinal atrophy resulting in a malabsorption syndrome known as celiac disease. However, gluten sensitivity may involve several organs and is often associated with extraintestinal manifestations. Typically, patients with celiac disease have circulating anti-tissue transglutaminase and anti-gliadin antibodies. When patients with gluten sensitivity are affected by other autoimmune diseases, other autoantibodies may arise like anti-epidermal transglutaminase in dermatitis herpetiformis, anti-thyroid peroxidase antibodies in thyroiditis, and anti-islet cells antibodies in type 1 diabetes. The most common neurological manifestation of gluten sensitivity is ataxia, the so-called gluten ataxia (GA). In patients with GA we have demonstrated that anti-gliadin and anti-tissue transglutaminase antibodies cross-react with neurons but that additional anti-neural antibodies are present. The aim of the present article is to review the knowledge on animal models of gluten sensitivity, as well as reviewing the role of anti-neural antibodies in GA.
Boscolo
Sabrina
S
BRAIN Centre for Neuroscience, Department of Biology, University of Trieste, Via Giorgieri 10, 34127 Trieste, Italy. sboscolo@units.it
Sarich
Alessandra
A
Lorenzon
Andrea
A
Passoni
Monica
M
Rui
Veronica
V
Stebel
Marco
M
Sblattero
Daniele
D
Marzari
Roberto
R
Hadjivassiliou
Marios
M
Tongiorgi
Enrico
E
D000818:Animals; D001259:Ataxia / Q000097:blood / Q000276:immunology* / Q000473:pathology; D001323:Autoantibodies / Q000097:blood / Q000276:immunology; D001522:Behavior, Animal; D004195:Disease Models, Animal; D005983:Glutens / Q000276:immunology*; D006801:Humans; D051379:Mice; D012680:Sensitivity and Specificity