Differentiation and effects of TGF-β1 and IL-3 signaling on primary murine endoglin deficient mast cells

Background: Mast cells (MCs) are components of the innate immune system and are recruited to the inflamed and fibrotic liver [1]. Mast cell effects are in part based on the secretion of mitogenic and pro-fibrotic cytokines (e.g. TGF-β1) leading to activation and proliferation of fibroblasts [2]. Nevertheless, MCs themselves are targets of TGF-β1 and do express the accessory TGF-β receptor endoglin with yet unknown function in MCs [3].