ArticleClinical & translational immunology2026
Aberrant intra-epithelial lymphocytes cause enterocyte cell death in refractory celiac disease by CD103-β7-receptor-mediated granzyme-B degranulation which can be restored by etrolizumab.
Article in Clinical & translational immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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19 authors.
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Abstract
Objectives: Refractory celiac disease type II (RCDII) is an intestinal tumor of aberrant intra-epithelial T-lymphocytes (IEL). The severe enteropathy found in RCDII is caused by aberrant IEL that exert cytotoxicity against enterocytes. In this study, we investigated the cell death mechanism responsible for villous atrophy in RCDII. Methods: Aberrant IEL were isolated from duodenal biopsies of RCDII patients. Enterocyte and RCDII patient-derived cell lines and human small intestinal organoids were used. mRNA expression was determined with reverse transcriptase-multiplex ligation-dependent probe amplification. Protein expression, degranulation and enterocyte killing were measured using flow cytometry, immunofluorescence or bright field microscopy. Secretion of granzyme-B was detected by enzyme immunoassay. Results: Levels of granzyme-B expression were significantly upregulated in aberrant IEL of RCDII patients compared to patients with celiac disease (CD) on gluten-free diet ( Conclusion: Killing of enterocytes in RCDII patients depends on degranulation of granzyme-B by aberrant IEL through CD103-β7 binding. By blocking this interaction, etrolizumab restores the intestinal epithelium and therefore should be considered as potential therapy for RCDII patients.
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