This presentation concerns the nature of the lesions in the smaller conducting airways less than 2 mm in internal diameter, which become the major site of airway obstruction in chronic obstructive pulmonary disease (COPD)(1–3). The 2-mm airways are located between the 4th and the 14th generation of tracheobronchial tree branching, depending on the length of the pathway followed (4). Unpublished data from our laboratory on more than 200 cases suggest that 80% of the conducting airways beyond this point are nonrespiratory bronchioles and the remaining 20% are smaller bronchi identified by the cartilage in their walls. Both the total number of airways and their collective crosssectional area increase rapidly in this region of the lung (4), and although there has been controversy about their contribution to the resistance to airflow in the normal lung (2), there is complete agreement that they become the major site of obstruction in COPD (1–3). The tobacco smoking habit is associated with a chronic inflammatory immune response in the lungs of every smoker and this response increases substantially in those who develop COPD (5, 6). It is also associated with the appearance of lymphoid follicles that document the presence of an adaptive immune response that increases sharply in severe (GOLD [Global Initiative for Chronic Obstructive Lung Disease] stage 3) and very severe (GOLD stage 4) COPD (5). A multivariate analysis of all of the data collected on these airways, however, showed that airflow limitation was most closely associated with the severity of the lumen occlusion by inflammatory exudates and the thickening of the walls of the small airways by a repair and remodeling process (5). The purpose of this presentation is to briefly review the nature of these inflammatory immune repair and remodeling processes as a basis for discussing the nature of the pathology at the site of airway obstruction in persons with COPD.