Biological treatments for asthma and chronic obstructive pulmonary disease

Asthma and chronic obstructive pulmonary disease (COPD) are highly prevalent heterogeneous airway diseases in which a subset of patients with severe disease have a disproportionate share of morbidity and mortality, largely through exacerbations. Major immunological advances have reframed both conditions around endotypes, with type 2 (inflammation driven by type 2 helper cells and group 2 innate lymphoid cells) and other inflammatory pathways defined and targeted with biological treatments. This review provides an overview of biological treatments in asthma and COPD. Biological treatments are engineered monoclonal antibodies targeting proteins (eg, IgE, interleukin (IL) 5 and IL5 receptor, IL4 and IL13, and upstream epithelial alarmins, such as thymic stromal lymphopoietin (TSLP) and IL33) that enable precision treatment. Biological treatments consistently reduce exacerbations and improve lung function and quality of life in biomarker defined populations. In asthma, short term biomarkers (blood eosinophils, fractional exhaled nitric oxide (FeNO), and sputum eosinophils) guide selection, whereas emerging longer term markers, including transcriptomic signatures and imaging endpoints, offer mechanistic readouts and raise the prospect of disease modification. In COPD, type 2 biological medicines have yielded benefits among patients with high levels of eosinophils and who are prone to exacerbations, and anti-IL33 and TSLP treatments show mixed but intriguing signals. Blood eosinophil counts (≥300 cells/µL) remain the most robust predictor of benefit; FeNO may provide complementary categorisation in select settings. Priorities for treatment are identifying treatable traits, supporting comprehensive self-management, and timely referral for patients with exacerbations despite optimised inhaled treatment. Key gaps include head-to-head comparisons, criteria for switching or stopping biological medicines, feasibility of de-escalation of inhaled treatment, and type 2 low strategies.