There has been an increased understanding, over the past 2 decades, that asthma is a chronic, immunologically mediated condition with a disturbance of the normal airway repair mechanism, which results in inflammatory changes and airway remodeling. The airway inflammation and remodeling together likely explain the clinical manifestations of asthma. The mechanisms by which the external environmental cues, together with the complex genetic actions, propagate the inflammatory process that characterize asthma are beginning to be understood. There is also an evolving awareness of the active participation of structural elements, such as the airway epithelium, airway smooth muscle, and endothelium, in this process. In tandem with this has come the realization that inflammatory cells respond in a coordinated, albeit dysfunctional manner, via an array of complex signaling pathways that facilitate communication between these cells; these structural elements within the lung and the bone marrow serve as reservoirs for and the source of inflammatory cells and their precursors. Although often viewed as separate mechanistic entities, so-called innate and acquired immunity often overlap in the propagation of the asthmatic response. This review examines the newer information on the pathophysiologic characteristics of asthma and focuses on papers published over the past 3 years that have helped to improve current levels of understanding.