• Understand that COPD is a lung disease with systemic involvement and consequences.

• Appreciate that these systemic manifestations significantly affect the outcomes and prognosis of both COPD, as well as of associated co-existent conditions.

• Be familiar with emerging tools/indices intended to help us better understand, appreciate, and manage these systemic manifestations and interactions.

No biologic treatments are currently available for type 2–low severe asthma, which is characterized by neutrophilic or paucigranulocytic airway inflammation and is associated with: older age, adult-onset asthma, obesity, metabolic syndrome, hypertension, and greater resistance to treatment with glucocorticoids. Although the pathophysiologic features of type 2–low asthma still need to be elucidated, several molecular mechanisms have been implicated, including interleukin-6, CXCL8 (CXC motif chemokine ligand 8), interleukin-17A, interleukin-23, interferon-γ, tumor necrosis factor-α, interleukin-33, and TSLP. Recently, the anti-TSLP antibody tezepelumab was shown to reduce exacerbation rates among patients with severe, uncontrolled asthma, irrespective of the blood eosinophil count at baseline, 51 whereas the anti–interleukin-23 monoclonal antibody risankizumab did not provide a clinical benefit in patients with severe asthma.