ArticlePloS one2017
Immunopathology of childhood celiac disease-Key role of intestinal epithelial cells.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 64 citations in OpenAlex.
- Genome-Wide Transcriptomic Analysis of Intestinal Mucosa in Celiac Disease Patients on a Gluten-Free Diet and Postgluten Challenge.Cellular and molecular gastroenterology and hepatology · 2021Trial
- T cell receptors for antigen on intraepithelial cytolytic T lymphocytes in celiac disease engage enterocyte HLA-E and HLA-B.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Article
- The SPINK Protein Family in Cancer: Emerging Roles in Tumor Progression, Therapeutic Resistance, and Precision Oncology.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Review
- PTGER4 signaling regulates class IIa HDAC function and SPINK4 mRNA levels in rectal epithelial cells.Cell communication and signaling : CCS · 2024Article
- PMF-GRN: a variational inference approach to single-cell gene regulatory network inference using probabilistic matrix factorization.Genome biology · 2024Article
- Salivary interleukin-17A and interleukin-18 levels in patients with celiac disease and periodontitis.PeerJ · 2024Article
- NOD-like Receptor Signaling Pathway in Gastrointestinal Inflammatory Diseases and Cancers.International journal of molecular sciences · 2023Review
- Transcriptome profile and immune infiltrated landscape revealed a novel role of γδT cells in mediating pyroptosis in celiac disease.Journal of translational medicine · 2023Article
- SPINK4 promotes colorectal cancer cell proliferation and inhibits ferroptosis.BMC gastroenterology · 2023Article
- Role of nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 6 in activation of inflammation in human umbilical vein endothelial cells stimulated byJournal of dental sciences · 2023Article
- Functional implications of the CpG island methylation in the pathogenesis of celiac disease.Molecular biology reports · 2022Review
- Pivotal Role of Inflammation in Celiac Disease.International journal of molecular sciences · 2022Review
- Inflammation Is Present, Persistent and More Sensitive to Proinflammatory Triggers in Celiac Disease Enterocytes.International journal of molecular sciences · 2022Article
- NOD-like receptors in autoimmune diseases.Acta pharmacologica Sinica · 2021Review
- Programmed Cell Death in the Small Intestine: Implications for the Pathogenesis of Celiac Disease.International journal of molecular sciences · 2021Review
- Article
- Identification of Neuropeptides as Potential Crosstalks Linking Down Syndrome and Periodontitis Revealed by Transcriptomic Analyses.Disease markers · 2021Article
- mTOR sustains inflammatory response in celiac disease.Scientific reports · 2020Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND &
aimsCeliac disease is a chronic inflammatory disease of the small intestine mucosa due to permanent intolerance to dietary gluten. The aim was to elucidate the role of small intestinal epithelial cells in the immunopathology of celiac disease in particular the influence of celiac disease-associated bacteria.
methodsDuodenal biopsies were collected from children with active celiac disease, treated celiac disease, and clinical controls. Intestinal epithelial cells were purified and analyzed for gene expression changes at the mRNA and protein levels. Two in vitro models for human intestinal epithelium, small intestinal enteroids and polarized tight monolayers, were utilized to assess how interferon-γ, interleukin-17A, celiac disease-associated bacteria and gluten influence intestinal epithelial cells.
resultsMore than 25 defense-related genes, including IRF1, SPINK4, ITLN1, OAS2, CIITA, HLA-DMB, HLA-DOB, PSMB9, TAP1, BTN3A1, and CX3CL1, were significantly upregulated in intestinal epithelial cells at active celiac disease. Of these genes, 70% were upregulated by interferon-γ via the IRF1 pathway. Most interestingly, IRF1 was also upregulated by celiac disease-associated bacteria. The NLRP6/8 inflammasome yielding CASP1 and biologically active interleukin-18, which induces interferon-γ in intraepithelial lymphocytes, was expressed in intestinal epithelial cells.
conclusionA key factor in the epithelial reaction in celiac disease appears to be over-expression of IRF1 that could be inherent and/or due to presence of undesirable microbes that act directly on IRF1. Dual activation of IRF1 and IRF1-regulated genes, both directly and via the interleukin-18 dependent inflammasome would drastically enhance the inflammatory response and lead to the pathological situation seen in active celiac disease.
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