ArticleCommunications biology2019
Constitutive alterations in vesicular trafficking increase the sensitivity of cells from celiac disease patients to gliadin.
Article in Communications biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.
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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.
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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, 24 citations in OpenAlex.
- Pediatric Celiac Disease Patients Show Alterations of Dendritic Cell Shape and Actin Rearrangement.International journal of molecular sciences · 2021Trial
- Proteomic Analysis Highlights Peculiar Protein and Phosphoprotein Profiles in Dermal Fibroblasts from Celiac Disease Patients.International journal of molecular sciences · 2026Article
- Innate immune dysregulation in celiac disease and refractory celiac disease: mechanisms, management and emerging therapies.Frontiers in immunology · 2026Review
- From gluten to therapeutics: molecular mechanisms of celiac disease and emerging alternatives to the gluten-free diet.Frontiers in pharmacology · 2026Review
- Review
- A Systems Biology Approach to the Pathogenesis of Celiac Disease: Identification of Potential Protective and Promoting Mechanisms.Advanced biomedical research · 2024Article
- Review
- Peculiar CaInternational journal of molecular sciences · 2023Article
- Article
- Review
- Type 2 Transglutaminase in Coeliac Disease: A Key Player in Pathogenesis, Diagnosis and Therapy.International journal of molecular sciences · 2022Review
- Pivotal Role of Inflammation in Celiac Disease.International journal of molecular sciences · 2022Review
- Gluten consumption and inflammation affect the development of celiac disease in at-risk children.Scientific reports · 2022Article
- Inflammation Is Present, Persistent and More Sensitive to Proinflammatory Triggers in Celiac Disease Enterocytes.International journal of molecular sciences · 2022Article
- Diosmectite inhibits the interaction between SARS-CoV-2 and human enterocytes by trapping viral particles, thereby preventing NF-kappaB activation and CXCL10 secretion.Scientific reports · 2021Article
- A Cumulative Effect of Food and Viruses to Trigger Celiac Disease (CD): A Commentary on the Recent Literature.International journal of molecular sciences · 2021Review
- Interplay Between Gluten, HLA, Innate and Adaptive Immunity Orchestrates the Development of Coeliac Disease.Frontiers in immunology · 2021Review
- Interplay between Type 2 Transglutaminase (TG2), Gliadin Peptide 31-43 and Anti-TG2 Antibodies in Celiac Disease.International journal of molecular sciences · 2020Review
- Constitutive Differential Features of Type 2 Transglutaminase in Cells Derived from Celiac Patients and from Healthy Subjects.International journal of molecular sciences · 2020Article
- Deciphering GRINA/Lifeguard1: Nuclear Location, CaInternational journal of molecular sciences · 2019Review
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Celiac Disease (CD) is an autoimmune disease characterized by inflammation of the intestinal mucosa due to an immune response to wheat gliadins. Some gliadin peptides (e.g., A-gliadin P57-68) induce an adaptive Th1 pro-inflammatory response. Other gliadin peptides (e.g., A-gliadin P31-43) induce a stress/innate immune response involving interleukin 15 (IL15) and interferon α (IFN-α). In the present study, we describe a stressed/inflamed celiac cellular phenotype in enterocytes and fibroblasts probably due to an alteration in the early-recycling endosomal system. Celiac cells are more sensitive to the gliadin peptide P31-43 and IL15 than controls. This phenotype is reproduced in control cells by inducing a delay in early vesicular trafficking. This constitutive lesion might mediate the stress/innate immune response to gliadin, which can be one of the triggers of the gliadin-specific T-cell response.
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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.