IL17A and chronic obstructive pulmonary disease: COPD has been associated with an increased IL-17 response directed against innocuous antigens.2 IL-17 promotes chronic airway inflammation by primarily acting on the lung epithelium through the upregulation of proinflammatory cytokines and chemokines.3,4 Genetic deletion of IL-17A attenuated cigarette smoke-induced inflammation and alveolar type 2 apoptosis in mice.5 The expression of IL-17A in human bronchial submucosa was significantly increased in patients with COPD compared with healthy control subjects and normal smokers.6,7