ArticleJCI insight2017
Stereotyped antibody responses target posttranslationally modified gluten in celiac disease.
Article in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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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
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- European Society for the Study of Coeliac Disease 2025 Updated Guidelines on the Diagnosis and Management of Coeliac Disease in Adults. Part 1: Diagnostic Approach.United European gastroenterology journal · 2025Guideline
- Changes in Non-Deamidated versus Deamidated Epitope Targeting and Disease Prediction during the Antibody Response to Gliadin and Transglutaminase of Infants at Risk for Celiac Disease.International journal of molecular sciences · 2022Trial
- Naïve adaptive immune receptor repertoires in celiac disease assessed by machine learning; impact of the HLA-DQ2.5 allotype on the TCR repertoire.Immunogenetics · 2026Article
- Machine Learning of Personal Repertoires From Public T Cell Receptors.Immunological reviews · 2026Review
- Harnessing gut microbiome enzymes:Microbiology spectrum · 2026Article
- High-throughput, quantitative approach to peptide epitope discovery.Medical & biological engineering & computing · 2026Article
- Immunoglobulin gene polymorphisms shape the naïve B-cell receptor repertoire; relevance to celiac disease.Genes and immunity · 2026Article
- Gut mucosal immune responses - Implications for celiac disease and food allergy.Seminars in immunology · 2025Review
- Enzyme-activating B-cell receptors boost antigen presentation to pathogenic T cells in gluten-sensitive autoimmunity.Nature communications · 2025Article
- New Insights on Genes, Gluten, and Immunopathogenesis of Celiac Disease.Gastroenterology · 2024Review
- 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
- Computational identification of HCV neutralizing antibodies with a common HCDR3 disulfide bond motif in the antibody repertoires of infected individuals.Nature communications · 2022Review
- Single-cell approaches to dissect adaptive immune responses involved in autoimmunity: the case of celiac disease.Mucosal immunology · 2022Review
- Immunoglobulin germline gene variation and its impact on human disease.Genes and immunity · 2021Review
- Gamma-gliadin specific celiac disease antibodies recognize p31-43 and p57-68 alpha gliadin peptides in deamidation related manner as a result of cross-reaction.Amino acids · 2021Article
- Article
- Longevity, clonal relationship, and transcriptional program of celiac disease-specific plasma cells.The Journal of experimental medicine · 2021Article
- Machine Learning Analysis of Naïve B-Cell Receptor Repertoires Stratifies Celiac Disease Patients and Controls.Frontiers in immunology · 2021Article
- TG2-gluten complexes as antigens for gluten-specific and transglutaminase-2 specific B cells in celiac disease.PloS one · 2021Article
- Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
The role of B cells and posttranslational modifications in pathogenesis of organ-specific immune diseases is increasingly envisioned but remains poorly understood, particularly in human disorders. In celiac disease, transglutaminase 2-modified (TG2-modified; deamidated) gluten peptides drive disease-specific T cell and B cell responses, and antibodies to deamidated gluten peptides are excellent diagnostic markers. Here, we substantiate by high-throughput sequencing of IGHV genes that antibodies to a disease-specific, deamidated, and immunodominant B cell epitope of gluten (PLQPEQPFP) have biased and stereotyped usage of IGHV3-23 and IGHV3-15 gene segments with modest somatic mutations. X-ray crystal structures of 2 prototype IGHV3-15/IGKV4-1 and IGHV3-23/IGLV4-69 antibodies reveal peptide interaction mainly via germline-encoded residues. In-depth mutational analysis showed restricted selection and substitution patterns at positions involved in antigen binding. While the IGHV3-15/IGKV4-1 antibody interacts with Glu5 and Gln6, the IGHV3-23/IGLV4-69 antibody interacts with Gln3, Pro4, Pro7, and Phe8 - residues involved in substrate recognition by TG2. Hence, both antibodies, despite different interaction with the epitope, recognize signatures of TG2 processing that facilitates B cell presentation of deamidated gluten peptides to T cells, thereby providing a molecular framework for the generation of these clinically important antibodies. The study provides essential insight into the pathogenic mechanism of celiac disease.
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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.