Gluten ataxia: passive transfer in a mouse model.

Abstract:

: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.

journal_name

Ann N Y Acad Sci

authors

Boscolo S,Sarich A,Lorenzon A,Passoni M,Rui V,Stebel M,Sblattero D,Marzari R,Hadjivassiliou M,Tongiorgi E

doi

10.1196/annals.1381.034

subject

Has Abstract

pub_date

2007-06-01 00:00:00

pages

319-28

eissn

0077-8923

issn

1749-6632

pii

1107/1/319

journal_volume

1107

pub_type

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