Cigarette smoke-driven antigens, bacterial or viral agents, breakdown products from extracellular matrix, and possibly lung tissue autoantigens can elicit adaptive immune responses in the lungs of COPD patients, with the participation of cytotoxic CD8+ T cells, T helper 1 and Th17 CD4+ cells [76, 77], and B-cell responses with antibody production [78]. This evidence concerns the gene CD8A and chronic obstructive pulmonary disease.