A sthma is a complex disorder characterized by intermittent, reversible airway obstruction, and by airway hyperresponsiveness and inflammation. Although its cause (s) remain unknown, we now recognize that asthma is a syndrome whose common pathologic expression is inflammation of the airways. The airways of patients with even mild asthma are inflamed, and some data suggest that the severity of the asthma parallels the degree of inflammation (1-3). The airway inflammation of asthma is unique in that the airway wall is infiltrated by T lymphocytes bearing the T helper type 2 phenotype (4) and by eosinophils and mast ceils (2, 5, 6). Each of these cells is thought to contribute to the physiologic changes that characterize asthma (Fig. 1). The TH2 lymphocytes produce a limited panel ofcytokines including IL-3, IL-4, IL-5, and GM-CSF. Although the primary signals resulting in the infiltration of the asthmatic airways by this lymphocyte subset have not yet been identified, a number of models have been proposed based on the concept that the inflammtory process is triggered by the presentation of a restricted panel of antigens in the presence of appropriate cytokines. The net effect of antigen presentation in this microenvironment is to promote the synthesis of IgE through the actions of IL-4 on Ig isotype switching (7) and to enhance the differentiation, migration, and pathobiologic capacity of eosinophils through the actions of GMCSF, IL-3, and IL-5 (8, 9). The IgE produced in asthmatic airways binds to Fc~ RI on mast cells, priming them for activation by antigen. Mast cells arise from bone marrow precursors, enter the circulation as non-metachromatically staining, agranular, CD34+, c-kit+, and F% I< I+ mononuclear leukocytes (10), and localize to mucosal and submucosal sites such as the bronchi. Once localized, these lineage-committed immature mast cells undergo tissue-specific differentiation along with maturation and expansion. Their development and movement involves growth factors and cytokines derived from both structural and hematopoietic cells in their microenvironment. The mast cells that further migrate into the luminal space, and which can be recovered by bronchoalveolar lavage, are primed for an augmented activation response (11). Mast cells also elaborate IL-4 (12, 13), which favors conversion ofT cells to the TH 2 phenotype, and IL-5 (14), which contributes to eosinophilopoiesis and to the priming of eosinophils for augmented responses. Once recruited from the circulation, mature eosinophils, in the presence of" asthmatic" cytokines, convert to an autoaggressive phenotype (15, 16), termed" hy-