CD4 and chronic obstructive pulmonary disease: Since the pulmonary inflammatory response and oxidative stress contribute to the development of COPD and our previous study showed that the methylation levels of the perforin gene promoter in CD4 + T lymphocytes were reduced and the AI of apoptotic alveolar septal cells was greater in rat models of autoimmune emphysema than in the normal group [8], we hypothesize that hypomethylation of the perforin gene promoter in CD4 + T lymphocytes are involved in alveolar septal cell apoptosis and that airway inflammation and oxidative stress play important roles in autoimmune emphysema in rats.