IGHE and airway hyperresponsiveness: These mediators play central roles in type 2 inflammation: IL-5 promotes eosinophil maturation and survival; IL-4 and IL-13 drive IgE class switching, mucus production, and airway hyperresponsiveness; IgE mediates allergic sensitization and mast-cell activation; and TSLP acts as an upstream epithelial cytokine that amplifies multiple inflammatory pathways [33].