ArticleJournal of immunology (Baltimore, Md. : 1950)2015
Igs as Substrates for Transglutaminase 2: Implications for Autoantibody Production in Celiac Disease.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 37 citations in OpenAlex.
- Human Transglutaminases: Updated Insights into Activation Mechanisms, Allosteric Regulation and Disease.International journal of molecular sciences · 2026Review
- Enzyme-activating B-cell receptors boost antigen presentation to pathogenic T cells in gluten-sensitive autoimmunity.Nature communications · 2025Article
- Autoantibody binding and unique enzyme-substrate intermediate conformation of human transglutaminase 3.Nature communications · 2023Article
- Secondary IgA Nephropathy and IgA-Associated Nephropathy: A Systematic Review of Case Reports.Journal of clinical medicine · 2023Review
- Infant antibody and B-cell responses following confirmed pediatric GII.17 norovirus infections functionally distinguish GII.17 genetic clusters.Frontiers in immunology · 2023Article
- Transglutaminase 2 affinity and enzyme-substrate intermediate stability as determining factors for T-cell responses to gluten peptides in celiac disease.European journal of immunology · 2022Article
- Comprehensive analysis of transglutaminase substrate preference by cDNA display coupled with next-generation sequencing and bioinformatics.Scientific reports · 2022Article
- Type 2 Transglutaminase in Coeliac Disease: A Key Player in Pathogenesis, Diagnosis and Therapy.International journal of molecular sciences · 2022Review
- Article
- Identification of Isopeptides Between Human Tissue Transglutaminase and Wheat, Rye, and Barley Gluten Peptides.Scientific reports · 2020Article
- Intestinal Anti-tissue Transglutaminase2 Autoantibodies: Pathogenic and Clinical Implications for Celiac Disease.Frontiers in nutrition · 2020Review
- Comprehensive Detection of Isopeptides between Human Tissue Transglutaminase and Gluten Peptides.Nutrients · 2019Article
- Plasma Cells Are the Most Abundant Gluten Peptide MHC-expressing Cells in Inflamed Intestinal Tissues From Patients With Celiac Disease.Gastroenterology · 2019Article
- 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
- 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
- Transglutaminase-2 promotes metastatic and stem-like phenotypes in osteosarcoma.American journal of cancer research · 2018Article
- Strong Clonal Relatedness between Serum and Gut IgA despite Different Plasma Cell Origins.Cell reports · 2017Article
- The roles of MHC class II genes and post-translational modification in celiac disease.Immunogenetics · 2017Review
- T Cells in Celiac Disease.Journal of immunology (Baltimore, Md. : 1950) · 2017Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Autoantibodies specific for the enzyme transglutaminase 2 (TG2) are a hallmark of the gluten-sensitive enteropathy celiac disease. Production of the Abs is strictly dependent on exposure to dietary gluten proteins, thus raising the question how a foreign Ag (gluten) can induce an autoimmune response. It has been suggested that TG2-reactive B cells are activated by gluten-reactive T cells following receptor-mediated uptake of TG2-gluten complexes. In this study, we propose a revised model that is based on the ability of the BCR to serve as a substrate to TG2 and become cross-linked to gluten-derived peptides. We show that TG2-specific IgD molecules are preferred in the reaction and that binding of TG2 via a common epitope targeted by cells using the IgH variable gene segment (IGHV)5-51 results in more efficient cross-linking. Based on these findings we hypothesize that IgD-expressing B cells using IGHV5-51 are preferentially activated, and we suggest that this property can explain the previously reported low number of somatic mutations as well as the overrepresentation of IGHV5-51 among TG2-specific plasma cells in the celiac lesion. The model also couples gluten peptide uptake by TG2-reactive B cells directly to peptide deamidation, which is necessary for the activation of gluten-reactive T cells. It thereby provides a link between gluten deamidation, T cell activation, and the production of TG2-specific Abs. These are all key events in the development of celiac disease, and by connecting them the model may explain why the same enzyme that catalyzes gluten deamidation is also an autoantigen, something that is hardly coincidental.
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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.