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Updated: Sep 1, 2025

A TNBS-Induced Rodent Model to Study the Pathogenic Role of Mechanical Stress in Crohn's Disease
Published on: March 1, 2022
Targeting CRAC channels in inflammatory bowel disease
Sven Kappel1, Christine Peinelt1
1Institute of Biochemistry and Molecular Medicine, University of Bern, Bern, Switzerland.
Abstract:
Inflammatory bowel disease (IBD) is a collective term for inflammatory diseases of the human gastrointestinal (GI) tract that are characterized by perturbations in the intestinal immune responses. In their study, Letizia et al (2022) found an enrichment of CD4+ effector T cells, interferon gamma (IFNγ) producing CD8+ T cells, regulatory T cells, and innate lymphoid cells (ILC) in the lamina propria (LP) of IBD patients. In these cells, pharmacological inhibition of store-operated calcium entry (SOCE) reduced cytokine production. In addition, in a murine IBD model, systemic SOCE inhibition reduced IBD severity and weight loss.
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