ArticleJournal of immunology (Baltimore, Md. : 1950)2011
Sensitization to gliadin induces moderate enteropathy and insulitis in nonobese diabetic-DQ8 mice.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 73 citations in OpenAlex.
- Article
- Targeted enzymatic therapy for coeliac disease.EMBO molecular medicine · 2026Article
- Small intestinal microbial fiber metabolism dysfunction in celiac disease.Nature communications · 2026Article
- Gene-Environment Interactions in Celiac Disease: The Role of the Intestinal Epithelium.Lifestyle genomics · 2026Review
- New Insights on Genes, Gluten, and Immunopathogenesis of Celiac Disease.Gastroenterology · 2024Review
- Non-Host Factors Influencing Onset and Severity of Celiac Disease.Gastroenterology · 2024Review
- Tolerance-inducing therapies in coeliac disease - mechanisms, progress and future directions.Nature reviews. Gastroenterology & hepatology · 2024Review
- Nanosized Additives: Silicon Dioxide's Potential Role in Development of Food Sensitivities in Mice.Environmental health perspectives · 2024Article
- Evaluating the Effects of Chronic Oral Exposure to the Food Additive Silicon Dioxide on Oral Tolerance Induction and Food Sensitivities in Mice.Environmental health perspectives · 2024Article
- Transcriptome-wide analysis reveals gluten-induced suppression of small intestine development in young chickens.Journal of animal science and technology · 2022Article
- The double-edged sword of gut bacteria in celiac disease and implications for therapeutic potential.Mucosal immunology · 2022Review
- Article
- Gluten-free diet exposure prohibits pathobiont expansion and gluten sensitive enteropathy in B cell deficient JH-/- mice.PloS one · 2022Article
- Cystic fibrosis transmembrane conductance regulator (CFTR) and autophagy: hereditary defects in cystic fibrosisOncotarget · 2019Review
- Article
- Duodenal bacterial proteolytic activity determines sensitivity to dietary antigen through protease-activated receptor-2.Nature communications · 2019Article
- A pathogenic role for cystic fibrosis transmembrane conductance regulator in celiac disease.The EMBO journal · 2019Article
- Common ground: shared risk factors for type 1 diabetes and celiac disease.Nature immunology · 2018Review
- Celiac Disease: A Review of Current Concepts in Pathogenesis, Prevention, and Novel Therapies.Frontiers in pediatrics · 2018Review
- A Commensal Bifidobacterium longum Strain Prevents Gluten-Related Immunopathology in Mice through Expression of a Serine Protease Inhibitor.Applied and environmental microbiology · 2017Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 4 countries.
Funding
Abstract
Celiac disease (CD) is frequently diagnosed in patients with type 1 diabetes (T1D), and T1D patients can exhibit Abs against tissue transglutaminase, the auto-antigen in CD. Thus, gliadin, the trigger in CD, has been suggested to have a role in T1D pathogenesis. The objective of this study was to investigate whether gliadin contributes to enteropathy and insulitis in NOD-DQ8 mice, an animal model that does not spontaneously develop T1D. Gliadin-sensitized NOD-DQ8 mice developed moderate enteropathy, intraepithelial lymphocytosis, and barrier dysfunction, but not insulitis. Administration of anti-CD25 mAbs before gliadin-sensitization induced partial depletion of CD25(+)Foxp3(+) T cells and led to severe insulitis, but did not exacerbate mucosal dysfunction. CD4(+) T cells isolated from pancreatic lymph nodes of mice that developed insulitis showed increased proliferation and proinflammatory cytokines after incubation with gliadin but not with BSA. CD4(+) T cells isolated from nonsensitized controls did not response to gliadin or BSA. In conclusion, gliadin sensitization induced moderate enteropathy in NOD-DQ8 mice. However, insulitis development required gliadin-sensitization and partial systemic depletion of CD25(+)Foxp3(+) T cells. This humanized murine model provides a mechanistic link to explain how the mucosal intolerance to a dietary protein can lead to insulitis in the presence of partial regulatory T cell deficiency.
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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.