ArticleNature structural & molecular biology2020
T cell receptor cross-reactivity between gliadin and bacterial peptides in celiac disease.
Article in Nature structural & molecular biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 2 of them syntheses 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
56 citing papers in PubMed, 2 syntheses or guidelines pooled it, 122 citations in OpenAlex.
- Pooled it
- Is Helicobacter pylori Infection Associated with Celiac Disease? A Meta-analysis.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2022Pooled it
- IgA deficiency reveals a microbiota-dependent pathway to gluten sensitivity.Gut microbes · 2026Article
- Gliadin-specific CD4Science advances · 2026Article
- Thymic selection of the T cell receptor repertoire is biased toward autoimmunity in females.eLife · 2026Article
- Immune cell dynamics and mechanisms of epithelial injury in celiac disease.Frontiers in immunology · 2026Review
- Association of endocrine autoantibodies (anti-TPO, anti-GAD, anti-insulin) with histopathological severity in pediatric Celiac disease: a retrospective cohort study.BMC pediatrics · 2025Article
- Gut mucosal immune responses - Implications for celiac disease and food allergy.Seminars in immunology · 2025Review
- High-resolution analysis of the treated coeliac disease microbiome reveals strain-level variation.Gut microbes · 2025Article
- Serotonin modulation of metabolism and stress response in Pseudomonas fluorescens.BMC biology · 2025Article
- Integrated fecal macrogenomic and metabolomic analyses reveal celiac disease flora and metabolic profiles associated with Chinese populations.Journal of translational medicine · 2025Article
- Is the microbiome important in celiac disease?Journal of the Canadian Association of Gastroenterology · 2025Article
- Immuno-informatics voyage through molecular mimicry of Heat Shock Proteins: Potential IBD immunopathogenesis.PloS one · 2025Article
- Inflammatory Myopathies and Autoimmune Gluten-related Disorders: A Scoping Review of Pathophysiological Interconnections and Hypothesis.Recent advances in inflammation & allergy drug discovery · 2025Article
- Non-Host Factors Influencing Onset and Severity of Celiac Disease.Gastroenterology · 2024Review
- T-FINDER: A highly sensitive, pan-HLA platform for functional T cell receptor and ligand discovery.Science advances · 2024Article
- Influence of Microbiota on Tumor Immunotherapy.International journal of biological sciences · 2024Review
- Preclinical characterization of MTX-101: a novel bispecific CD8 Treg modulator that restores CD8 Treg functions to suppress pathogenic T cells in autoimmune diseases.Frontiers in immunology · 2024Article
- Characterizations of a neutralizing antibody broadly reactive to multiple gluten peptide:HLA-DQ2.5 complexes in the context of celiac disease.Nature communications · 2023Article
- Emerging Pharmaceutical Therapies to Address the Inadequacy of a Gluten-Free Diet for Celiac Disease.Pharmaceuticals (Basel, Switzerland) · 2023Review
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Authors and funding
15 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human leukocyte antigen (HLA) locus is strongly associated with T cell-mediated autoimmune disorders. HLA-DQ2.5-mediated celiac disease (CeD) is triggered by the ingestion of gluten, although the relative roles of genetic and environmental risk factors in CeD is unclear. Here we identify microbially derived mimics of gliadin epitopes and a parental bacterial protein that is naturally processed by antigen-presenting cells and activated gliadin reactive HLA-DQ2.5-restricted T cells derived from CeD patients. Crystal structures of T cell receptors in complex with HLA-DQ2.5 bound to two distinct bacterial peptides demonstrate that molecular mimicry underpins cross-reactivity toward the gliadin epitopes. Accordingly, gliadin reactive T cells involved in CeD pathogenesis cross-react with ubiquitous bacterial peptides, thereby suggesting microbial exposure as a potential environmental factor in CeD.
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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.