Chronic obstructive pulmonary disease (COPD) is a significant cause of morbidity and mortality worldwide. In contrast to other chronic diseases, COPD is increasing in prevalence and is projected to be the third leading cause of death and disability worldwide by 2030. Recent advances in understanding the underlying pathophysiology of COPD has led to the development of novel targeted therapies (biologics and small molecules) that address the underlying pathophysiology of the disease. In severe asthma, biologics targeting type 2 (T2)- mediated immunity have been successful and have changed the treatment paradigm. In contrast, no biologics are currently licensed for the treatment of COPD. Those targeting non-T2 pathways have not demonstrated efficacy and in some cases raised concerns related to safety. With the increasing recognition of the eosinophil and perhaps T2-immunity possibly playing a role in a subgroup of patients with COPD, T2 biologics, specifically anti–IL-5(R), have been tested and demonstrated modest reductions in exacerbation frequency. Potential benefit was related to the baseline blood eosinophil count. These benefits were small compared with asthma. Thus, whether a subgroup of COPD sufferers might respond to anti–IL-5 or other T2-directed biologics remains to be fully addressed and requires further investigation. Chronic obstructive pulmonary disease (COPD) is a significant cause of morbidity and mortality worldwide. In contrast to other chronic diseases, COPD is increasing in prevalence and is projected to be the third leading cause of death and disability worldwide by 2030. Recent advances in understanding the underlying pathophysiology of COPD has led to the development of novel targeted therapies (biologics and small molecules) that address the underlying pathophysiology of the disease. In severe asthma, biologics targeting type 2 (T2)- mediated immunity have been successful and have changed the treatment paradigm. In contrast, no biologics are currently licensed for the treatment of COPD. Those targeting non-T2 pathways have not demonstrated efficacy and in some cases raised concerns related to safety. With the increasing recognition of the eosinophil and perhaps T2-immunity possibly playing a role in a subgroup of patients with COPD, T2 biologics, specifically anti–IL-5(R), have been tested and demonstrated modest reductions in exacerbation frequency. Potential benefit was related to the baseline blood eosinophil count. These benefits were small compared with asthma. Thus, whether a subgroup of COPD sufferers might respond to anti–IL-5 or other T2-directed biologics remains to be fully addressed and requires further investigation. Biologics, Clinical Context, and the AsthmasThe Journal of Allergy and Clinical Immunology: In PracticeVol. 7Issue 5PreviewIt has been more than 15 years since the US Food and Drug Administration approved omalizumab for the therapy of moderate-to-severe perennial allergic asthma. The concept of removing one of the key triggers of asthma, IgE, excited the scientific and medical community. Indeed, with 80% of children and 50% of adults having a significant allergic trigger to their asthma, it was envisioned that this approach could lead to long-standing remission or perhaps even a cure for many patients. Moreover, serum IgE levels had been shown to be increased in smokers, implicating a potential role for IgE in the pathogenesis of smoking-related lung diseases such as chronic obstructive pulmonary disease (COPD). Full-Text PDF CME Exam: T2 Biologics for Chronic Obstructive Pulmonary DiseaseThe Journal of Allergy and Clinical Immunology: In PracticeVol. 7Issue 5Preview Full-Text PDF