Immunologic concepts of asthma and related allergic diseases are undergoing revolutionary changes. Research into immunologic mechanisms has typically focused on the acute anaphylactic component, that is, on the role of mast cells and immunoglobulin E. Briefly, when a multivalent allergen cross-links IgE molecules bound to high-affinity Fc epsilon receptors on the mast cell surface, the cells release chemical mediators that constrict the bronchi, dilate blood vessels, cause edema, and recruit eosinophils. Recent investigation, utilizing bronchoscopic lavage and biopsy and cell biology, is emphasizing chronic eosinophilic airway inflammation and is clarifying the mechanisms of a complex multicellular chain of reactions that involve not only mast cells and basophils, but lymphocytes, eosinophils, endothelial cells, and epithelial cells, and may also involve platelets, macrophages, and neutrophils. The airways contain activated TH2-like lymphocytes that release cytokines which recruit and activate eosinophils. These cytokines also generate adhesion molecules on endothelial cell surfaces that promote diapedesis of the eosinophils out of the circulation into the submucosa, mucosa, and lumen of the airway. In the tissues, the eosinophils degranulate, releasing toxic proteins that damage the respiratory epithelium and account for many of the histopathologic abnormalities of asthma.