Central drivers of type 2 inflammation interleukin (IL)-4 and IL-13 have unique and overlapping functions, contributing the pathophysiology of asthma, chronic rhinosinusitis with nasal polyps and allergic rhinitis [3, 31, 92, 93, 9399]

Th2 cell differentiationGoblet cell hyperplasiaEosinophil differentiation and survival
Mucociliary dysfunction
Excess mucus production
Collagen deposition
Smooth muscle proliferation
Increased contractility
Neuroimmune dysfunction
B-cell isotype switching and IgE production; mast cell and basophil degranulation
Mast cell activation and trafficking to tissue
Fibrosis and airway remodelling
Epithelial barrier dysfunction and microbiome imbalance
TARC-induced migration of Th2 cells
Activation of macrophages to M2 type
Eosinophil recruitment and trafficking to tissue

Th2: type 2 T-helper; TARC: thymus and activation-regulated chemokine.