Interleukin-13 (IL-13) is a Th2-derived cytokine central to type 2 immune responses, playing a key role in allergic inflammation, tissue remodeling, and host defense against parasites. It binds to receptors (IL-13Rα1/IL-4Rα and IL-13Rα2), activating JAK-STAT signaling pathways that drive eosinophil recruitment, mucus hypersecretion, and fibrosis. Dysregulated IL-13 signaling is implicated in chronic inflammatory diseases, including asthma, atopic dermatitis (AD), chronic rhinosinusitis with nasal polyps (CRSwNP), and eosinophilic esophagitis.
IL-13-targeting antibodies are biologic therapies designed to block this pathway. Most are monoclonal antibodies (mAbs) that either neutralize IL-13 directly or inhibit its receptor interactions. For example, lebrikizumab and tralokinumab bind IL-13. preventing receptor engagement, while dupilumab indirectly affects IL-13 signaling by blocking the shared IL-4Rα subunit. Clinical trials have shown efficacy in reducing exacerbations in severe asthma, improving skin lesions in AD, and decreasing nasal polyp size in CRSwNP. These therapies are particularly valuable for patients unresponsive to conventional treatments.
Despite promise, challenges remain. Patient heterogeneity in IL-13-driven pathologies necessitates biomarker-guided approaches (e.g., periostin levels) to optimize treatment response. Additionally, safety concerns like conjunctivitis in AD patients highlight the need for further mechanistic insights. Ongoing research explores combination therapies and next-generation bispecific antibodies targeting IL-13 alongside other mediators (e.g., IL-4. TSLP) to broaden efficacy. Overall, IL-13 antibodies represent a transformative approach for type 2 inflammation, with expanding applications across immune-mediated diseases.