Gluten ataxia: passive transfer in a mouse model

Ann N Y Acad Sci. 2007 Jun:1107:319-28. doi: 10.1196/annals.1381.034.


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.

Publication types

  • Review

MeSH terms

  • Animals
  • Ataxia / blood
  • Ataxia / immunology*
  • Ataxia / pathology
  • Autoantibodies / blood
  • Autoantibodies / immunology
  • Behavior, Animal
  • Disease Models, Animal
  • Glutens / immunology*
  • Humans
  • Mice
  • Sensitivity and Specificity


  • Autoantibodies
  • Glutens