Asthma and COPD are prevalent chronic inflammatory airway diseases that are 
responsible for a large global disease burden. Both diseases are complex and 
heterogeneous, and they are increasingly recognized as overlapping syndromes 
that may share similar pathophysiologic mechanisms and treatable traits. 
Eosinophilic airway inflammation is considered the most influential treatable 
trait of chronic airway disease, and over the last decade, several monoclonal 
antibodies and small molecule therapies have been developed to target this 
trait. These include monoclonal antibodies against IL-5 or IL-5 receptor alpha 
(mepolizumab, reslizumab, and benralizumab), IL-13 (lebrikizumab and 
tralokinumab), IL-4 receptor alpha (dupilumab), IgE (omalizumab), and 
anti-thymic stromal lymphopoietin (tezepelumab) and small molecule therapies 
such as prostaglandin D2 blockers (fevipiprant and timapiprant). Although these 
novel biologic agents have shown promising results in many patients with asthma 
and COPD who have eosinophilic airway inflammation, it is evident that not all 
patients respond equally well, despite similar clinical, functional, and 
inflammatory characteristics. This heterogeneity in treatment response is 
probably related to different molecular pathways or endotypes leading to 
eosinophilic airway inflammation, including adaptive immune pathways mediated by 
T helper 2 cells and innate immune pathways mediated by innate lymphoid cells. 
The relative contribution of these pathways in asthma and COPD is not yet 
clarified, and there are currently no reliable biomarkers that represent the 
various pathways. Therefore, there is an urgent need for easily measurable and 
reproducible biomarkers that are linked to underlying pathophysiologic disease 
mechanisms and can predict and monitor responses to novel biologic agents.