CD8A and chronic obstructive pulmonary disease: Recent studies, reviewed by Rovina et al. [12], have also shown that cigarette-smoke-driven agents (including antigens, lung tissue breakdown products, and/or autoantigens) may elicit adaptive immune responses in the lungs of COPD patients with the participation of cytotoxic CD8+ T cells, Th1, and Th17 CD4+ cells (and B cell responses with antibody production), and that the extent of airflow limitation and emphysema in COPD correlates with the number of pulmonary CD8+ T cells, which, upon activation, release proteolytic enzymes causing the death of structural cells by apoptosis or necrosis.