ArticlePloS one2010
Anti transglutaminase antibodies cause ataxia in mice.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 113 citations in OpenAlex.
- Pooled it
- Human Transglutaminases: Updated Insights into Activation Mechanisms, Allosteric Regulation and Disease.International journal of molecular sciences · 2026Review
- Epilepsy and coeliac disease in children: a narrative review.Frontiers in pediatrics · 2026Review
- Serological analysis of gluten-related antibodies in idiopathic neuropathies and cerebellar ataxia.Journal of neurology · 2025Article
- Recent advances in diagnosis of immune-mediated cerebellar ataxias: novel concepts and fundamental questions on autoimmune mechanisms.Journal of neurology · 2024Review
- Autoantibodies related to ataxia and other central nervous system manifestations of gluten enteropathy.World journal of clinical cases · 2024Review
- Evaluation of the Prevalence of Anti-transglutaminase 2 and 6 Antibodies in Patients with Sero-Positive Multiple Sclerosis.Middle East journal of digestive diseases · 2024Article
- Epilepsy, Immunity and Neuropsychiatric Disorders.Current neuropharmacology · 2023Review
- Type 2 Transglutaminase in Coeliac Disease: A Key Player in Pathogenesis, Diagnosis and Therapy.International journal of molecular sciences · 2022Review
- Acute Cerebellar Inflammation and Related Ataxia: Mechanisms and Pathophysiology.Brain sciences · 2022Review
- A Breakdown of Immune Tolerance in the Cerebellum.Brain sciences · 2022Review
- Neurological manifestation of coeliac disease with particular emphasis on gluten ataxia and immunological injury: a review article.Gastroenterology and hepatology from bed to bench · 2021Review
- Immune-Mediated Cerebellar Ataxias: Clinical Diagnosis and Treatment Based on Immunological and Physiological Mechanisms.Journal of movement disorders · 2021Article
- Neuroimmunogastroenterology: At the Interface of Neuroimmunology and Gastroenterology.Frontiers in neurology · 2020Review
- Transglutaminase 2 and Transglutaminase 2 Autoantibodies in Celiac Disease: a Review.Clinical reviews in allergy & immunology · 2019Review
- Stimulus Sensitive Foot Myoclonus: A Clue to Coeliac Disease.Movement disorders clinical practice · 2019Article
- Hispanic Spinocerebellar Ataxia Type 35 (SCA35) with a Novel Frameshift Mutation.Cerebellum (London, England) · 2019Article
- Immune-mediated Cerebellar Ataxias: Practical Guidelines and Therapeutic Challenges.Current neuropharmacology · 2019Review
- Anti-type 2 transglutaminase antibodies as modulators of type 2 transglutaminase functions: a possible pathological role in celiac disease.Cellular and molecular life sciences : CMLS · 2018Review
- Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundCeliac 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.
methodsWe 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.
conclusionThe serum from CD patients contains anti-TG2, TG3 and TG6 antibodies that may potentially cause ataxia.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.