IFN-γ stimulates Paneth cell secretion through necroptosis mTORC1 dependent.
Maria R Encarnacion-GarciaRaúl De la Torre-BaezMaría A Hernandez-CuetoLaura A Velázquez-VillegasAurora Candelario-MartinezAna Beatriz Sánchez-ArgáezPerla H Horta-LópezArmando Montoya-GarcíaGustavo Alberto Jaimes-OrtegaLuis Lopez-BailonZayda Piedra-QuinteroGabriela Carrasco-TorresMarlon De ItaMaría Del Pilar Figueroa-CoronaJosé Esteban Muñoz-MedinaMagdalena Sánchez-UribeArturo Ortiz-FernándezMarco Antonio Meraz-RiosAngélica Silva-OlivaresAbigail BetanzosGuillermina Juliana Baay-GuzmanFernando Navarro-GarciaSaúl Villa-TreviñoFrancisco Garcia-SierraBulmaro CisnerosMichael SchnoorVianney F Ortíz-NavarreteNicolas Villegas-SepulvedaRicardo Valle-RiosÓscar Medina-ContrerasLilia G NoriegaPorfirio NavaPublished in: European journal of immunology (2024)
Immune mediators affect multiple biological functions of intestinal epithelial cells (IECs) and, like Paneth and Paneth-like cells, play an important role in intestinal epithelial homeostasis. IFN-γ a prototypical proinflammatory cytokine disrupts intestinal epithelial homeostasis. However, the mechanism underlying the process remains unknown. In this study, using in vivo and in vitro models we demonstrate that IFN-γ is spontaneously secreted in the small intestine. Furthermore, we observed that this cytokine stimulates mitochondrial activity, ROS production, and Paneth and Paneth-like cell secretion. Paneth and Paneth-like secretion downstream of IFN-γ, as identified here, is mTORC1 and necroptosis-dependent. Thus, our findings revealed that the pleiotropic function of IFN-γ also includes the regulation of Paneth cell function in the homeostatic gut.