No abstract

Lung cancer is the second most common and the most lethal cancer worldwide, accounting for 11.6% of all new cancer cases and 19.8% of all cancer-related deaths. 1 Recent research has fostered new insights into lung cancer biology, and considerable progress has been made in the field of novel biomarker-targeted therapies, including molecular therapies targeting epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK) and proto-oncogene B-Raf (BRAF), 2,3 and immunotherapies with checkpoint inhibitors targeting the programmed cell death 1 (PD-1) and programmed death-ligand 1 (PD-L1) pathways. 4 However, lung cancer still has one of the lowest 5-year survival rates (only 18%) of all cancer types. 5 The high mortality is attributed to the fact that most lung cancers are diagnosed at advanced stages

We here show that the activity of the immunoproteasome is impaired by cigarette smoke resulting in reduced MHC I antigen presentation. Regulation of immunoproteasome function by cigarette smoke may thus alter adaptive immune responses and add to prolonged infections and exacerbations in COPD and IPF.