This review summarizes the pathophysiological mechanisms of type 2 inflammation in chronic obstructive pulmonary disease (COPD) and recent research advances in related biologic therapies. As a major global health burden, the therapeutic strategy for COPD is gradually shifting from symptom management towards precision medicine targeting the underlying pathophysiology. Key inflammatory mediators currently under investigation in type 2 inflammation in COPD include TSLP, IL-33, IL-4, IL-5, and IL-13, which play critical roles in the pathophysiological alterations of the disease. Biologics targeting type 2 inflammation, such as Tezepelumab (targeting thymic stromal lymphopoietin, TSLP), Itepekimab and Astegolimab (targeting IL-33), and Dupilumab (targeting IL-4/IL-13), have demonstrated potential in clinical trials to improve outcomes and enhance the quality of life for COPD patients. Although these biologics offer novel therapeutic options, issues regarding their long-term efficacy, safety, cost-effectiveness, and global accessibility require further investigation. This article systematically outlines the molecular mechanisms of type 2 inflammation in COPD and the progress in targeted therapies. It emphasizes that the clinical translation of biologics must be guided by precision medicine, integrating mechanistic research with real-world evidence to advance COPD treatment towards "individualized intervention." Future research needs to further elucidate the interactions between type 2 and non-type 2 inflammatory phenotypes and to explore combination therapeutic strategies, in order to provide more comprehensive solutions for the prevention and management of COPD.
Song et al. (Tue,) studied this question.