In the context of damaged airway epithelium as in CRSwNP, triggers that initiate and perpetuate type-2 inflammation may be different: viruses, bacteria, allergens, cigarette smoke, pollutants, etc. Yet, there is increasing evidence that viruses may enhance type-2 immunological response by stimulating the epithelial expression of the cytokines thymic stromal lymphopoietin (TSLP), IL-25, and IL-33. Here, TSLP is linked to chronic rhinosinusitis with nasal polyps.