ABSTRACT
Inflammation of the airway mucosa and submucosa is thought to play a major role in the pathogenesis of asthma (1,2). Although the inflammatory response is complex, airway CD4 Th2-type lymphocytes (Th2 cells), mast cells, basophils, and eosinophils appear to be the primary effector cells that orchestrate the clinical manifestations of disease. In particular, the infiltration of the airways by Th2 cells and eosinophils are predominant features of the late-phase asthmatic response. Indeed, the hallmark features of allergic asthma: elevated serum immunoglobulin E (IgE), mucus hypersecretion, eosinophilia, and enhanced bronchial reactivity [airways hyperreactivity (AHR)] to nonspecific spasmogenic stimuli have all been linked to the effector functions of Th2 cytokines [e.g., interleukin(IL)-4,-5,-9,-10, and -13] (2). Importantly, it is these pathogenic processes that are thought to promote airways obstruction in asthma, which predisposes to wheezing, shortness of breath, and life-threatening limitations in airflow. Although the etiology and pathophysiology of asthma are complex, a central paradigm in asthma pathogenesis has emerged whereby Th2 cells regulate disease processes through the recruitment and activation of eosinophils in the allergic lung. In this model, Th2 cells, through the secretion of IL-5, regulate eosinophil recruitment to the lung and thereby pathogenic processes that predispose to the development of airways obstruction and AHR.
