ReviewLifestyle genomics2026
Gene-Environment Interactions in Celiac Disease: The Role of the Intestinal Epithelium.
Review in Lifestyle genomics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCeliac disease (CeD) is a chronic, immune-mediated condition driven by dietary gluten in genetically predisposed individuals, primarily those carrying HLA-DQ2 and HLA-DQ8. Unlike other autoimmune diseases, CeD offers an exceptional degree of mechanistic clarity, stemming from the identification of the main environmental driver, gluten, and its link with genetic susceptibility. SUMMARY: While gluten and HLA genotype are necessary for developing CeD, they are not sufficient. Emerging research highlights that environmental and lifestyle factors, including early-life ecosystem, infections, and gut microbiota, critically modulate CeD risk and severity. This review synthesizes emerging insights and focuses on the role of the intestinal epithelium not just as target of immune-mediated injury but as an active interface integrating genetic susceptibility with environmental cues. Recent data reveal that intestinal epithelial cells can release tissue transglutaminase 2 that modifies gluten peptide antigenicity, participate in antigen presentation and immune signaling, and respond to microbial and dietary factors, positioning them as contributors to CeD initiation and progression. The review also highlights knowledge gaps and areas of active debate in CeD. KEY MESSAGES: CeD has a main environmental driver (gluten) and a defined genetic susceptibility, linked to major histocompatibility complex class II DQ2 and DQ8. Activation of the CD4+ T-cell response by gluten and cytotoxic transformation of intraepithelial lymphocytes culminate in villus atrophy of the proximal small intestine. In this opinion-based perspective, we integrate and review recent evidence suggesting the intestinal epithelium plays an active role in CeD initiation and/or progression, which could lead to strategies to prevent or better treat this condition.
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Registered trials
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