Mechanisms linking IFN-mediated cell death with bile acid signaling in small intestinal inflammation

Project Summary

Although interferons (IFNs) act at mucosal surfaces, the molecular mechanisms underlying their mucosal functions are still poorly understood. Our unpublished data suggest that IFN-induced programmed necrosis plays a key role in the pathogenesis of intestinal inflammation. Accordingly, IFNs promote non-apoptotic epithelial cell death, upregulation of the mixed lineage kinase domain-like protein, and disruption of immune homeostasis. The central question of this project is whether, and through which pathways, epithelial IFN-regulated necrosis contributes to intestinal inflammation. We aim to uncover new functions of IFNs in immune-epithelial communication that could become targets for future therapeutic interventions.

Selected project-relevant publications