BACKGROUND. Programmed Death Ligand 1 (PD-L1) is crucial in regulating the immunological tolerance in non-small cell lung cancer (NSCLC). PD-L1 behavior in COPD (a chronic lung adaptive inflammation with possible dysregulated immune tolerance) and how it could affect NSCLC is not clear.

AIM. To investigate PD-L1 expression in smokers with COPD (SCOPD), without COPD (noCOPD) and non-smokers (NS) with NSCLC and its relation to clinical and inflammatory features. 

METHODS. PD-L1 expression was quantified in lung tissue samples from 71 patients with NSCLC. Medical history, pulmonary function and blood cell counts were obtained. The possible relations of clinical data to PD-L1 values were investigated. 

RESULTS. 35 of the 71 NSCLC patients were SCOPD (FEV1 67±16%), 21 noCOPD (99±12%) and 15 NS (100±17%). PD-L1 tissue expression was higher in SCOPD (20 [5-56]%) than in smokers noCOPD (2 [0-21]%; p=0.05) and NS (1 [0-21]%; p=0.05). Squamous cell carcinoma was more common in SCOPD than NS (14/35 vs 1/15; p=0.02). PD-L1 expression was similar among cancer histotypes, genders, and cancer stage (advanced: 28±31%, early: 18±26%). PD-L1 was not related to pack-years, blood cell counts, or lung function. Overall, patients with FEV1<67% of predicted (25° percentile) had lower circulating lymphocytes (19±6 vs 26±8%; p=0.01) and higher NLR (4±3 vs 3±2; p=0.01) than those with higher FEV1.

CONCLUSIONS. PD-L1 was strikingly higher in smokers with NSCLC and COPD than in those without COPD, suggesting that dysregulation of adaptive immune response in COPD contributes to PD-L1 expression and might have beneficial therapeutic effects.