IL-13 is a pleiotropic cytokine that orchestrates type 2 immune responses and allergic inflammation through multiple signaling pathways. Functionally, IL-13 promotes B-cell proliferation and activates eosinophils, basophils, and mast cells 1, while inducing alternative activation of macrophages 1. The cytokine exerts its effects by binding to IL4R and IL13RA1 receptor chains to activate JAK1/TYK2 and STAT6 signaling 2, though IL13RA2 acts as a high-affinity decoy receptor that internalizes and depletes extracellular IL-13, providing negative regulation. Mechanistically, IL-13 drives pathological remodeling in airway diseases by inducing goblet cell differentiation and mucus hypersecretion 3, upregulating vascular cell adhesion molecule-1 (VCAM-1) for immune cell recruitment, and promoting smooth muscle hypertrophy 4. In chr5 rhinosinusitis with nasal polyps, IL-13 perpetuates type 2 inflammation by activating eosinophils, M2 macrophages, and B cells, leading to mucus overproduction and tissue remodeling 5. Clinically, IL-13 is central to allergic and type 2 inflammatory diseases. IL-13 targeting shows therapeutic promise: tralokinumab (anti-IL-13 monoclonal antibody) improved atopic dermatitis symptoms 6, while dupilumab (anti-IL-4Rα, blocking both IL-4/IL-13 signaling) reduces asthma exacerbations and improves lung function 4. Lunsekimig, a bispecific inhibitor targeting both TSLP and IL-13, demonstrated favorable pharmacokinetics and tolerability in clinical trials 7.