Abstract
Type 2 (T2) inflammation is a major pathogenic pathway in asthma and a clinically relevant endotype in a subgroup of patients with chronic obstructive pulmonary disease (COPD). This narrative review compares the mechanisms, biomarker-based assessment, and targeted treatment of T2 inflammation across these diseases. We focus on blood and sputum eosinophils, fractional exhaled nitric oxide (FeNO), and total and allergen-specific immunoglobulin E (IgE), while examining discordance among biomarkers and the effects of corticosteroids, smoking, infection, circadian variation, coexisting T2 diseases, and population- or assay-dependent thresholds. We distinguish the adjunctive role of biomarkers in diagnosis from their more established roles in phenotyping, risk stratification, and treatment selection. Evidence from pivotal trials is synthesized for established and recently approved therapies, including the jurisdiction-specific positioning of depemokimab in severe asthma and mepolizumab in eosinophilic COPD, while investigational strategies targeting epithelial alarmins and related pathways are critically appraised. We also discuss clinical remission as an evolving treatment goal. Overall, repeated multidimensional assessment integrating biomarkers with clinical characteristics, lung function, comorbidities, exacerbation history, and treatment exposure is more informative than any single threshold and may support more precise management of asthma and COPD.