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In drawing on studies that extend from clinical epidemiology, through genetics, pharmacotherapy and animal models, to cell biology and biochemistry, we have aimed to provide a comprehensible and accessible narrative, although this comes at the expense of a fully comprehensive and systematic (and inevitably longer) analysis

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The central hypothesis is that EECs contribute to the pathogenesis of inflammatory bowel diseases (IBD) due to their role in endocrine-immune crosstalk, particularly via GLP-1's influence on intraepithelial lymphocytes and metabolic-inflammatory responses