Abstract
Mast cells (MCs) are key effector cells that expand and participate in the pathophysiology of type 2 inflammatory disease, including asthma and chronic rhinosinusitis with nasal polyps (CRSwNP). MCs exhibit microenvironment-dependent protease phenotypes: in the airways and gut, sub-epithelial MCs co-express tryptase and chymase (MCTC), while those within epithelium mainly express tryptase alone (MCT). However, the signaling pathways driving these phenotypes are unclear. We previously identified a role for TGF-β signaling in directing murine MC intraepithelial airway phenotype and hypothesize that TGF-β plays a similar role for human MCs.
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