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To the Editor:
The interaction of programmed death receptor 1 (PD-1) with its corresponding ligand (PD-L1), an important inhibitory immune checkpoint, is currently a hot topic in pulmonary oncology. Inhibitors of PD-1, such as nivolumab or pembrolizumab, increase the endogenous inflammatory reaction against cancer cells (1). Clinical studies showed that these immune checkpoint inhibitors are more effective than conventional chemotherapy in fighting non-small cell lung cancer (NSCLC) (2, 3), resulting in an approval of these compounds for NSCLC treatment. The article in the Journal by McKendry and colleagues showed that the expression of PD-L1 on macrophages was reduced in patients with chronic obstructive pulmonary disease (COPD) (4). In addition, PD-L1 expression is also reduced on dendritic cells in COPD (5). The reduced PD-L1 expression on antigen-presenting cells has been postulated to play an important role in the pathogenesis of chronic airway inflammation in COPD. COPD is a very common comorbidity in patients with NSCLC (6). Despite the efficacy of PD-1 inhibitors in NSCLC, the adverse effects of these compounds in COPD are currently unknown. It might be speculated that a further inhibition of the impaired PD-1-PD-L1 axis in COPD could increase airway inflammation and thus promote disease progression. Therefore, the studies by McKendry and colleagues (4) and Stoll and colleagues (5) show that the beneficial effects of PD-1 inhibitors on NSCLC must be weighed against potential detrimental adverse effects on the comorbidity of COPD. Thus, further clinical and experimental studies are urgently needed to document that PD-1 inhibitor treatment is safe in patients with COPD. n
Author disclosures are available with the text of this letter at www.atsjournals.org.
Paul Stoll, M.D.
Johann Christian Virchow,...