Cigarette smoking is the main trigger for the development of chronic obstructive pulmonary disease (COPD). For years the inflammatory reaction in COPD was focused on neutrophils, macrophages and protease-antiprotease balance. The concept of inflammation has been changed since the findings in the bronchoalveolar lavage (BAL) of smokers and COPD patients. It is now evident that the inflammatory reaction composed of neutrophils and macrophages represents the innate immunity reaction. This reaction will proceed over time to damage the lung, producing peptides and modified proteins from matrix destruction, cell necrosis and cell apoptosis. These products have the potential to act as antigen determinants. Dendritic cells which are abundantly present in smokers' lungs are important link between innate and adaptive immunity involving T-cells. These cells mature and migrate to draining lymphatic organs, where they could present antigens to CD-4+ and CD-8+. T-cells that induce their activation and differentiation. As a result T-cells are important component of the chronic inflammation in smokers and in COPD patients. So one of the possible conclusions could be that COPD is a disease produced, at least in part, by self-antigens from the lung secondary to smoking.