We hypothesized that allergen-induced airway eosinophilia is linked to activation or recruitment of T cells in the airway and generation of interleukin-5 (IL-5). To evaluate this hypothesis, we performed bronchoscopy with segmental antigen bronchoprovocation in 12 atopic subjects. Bronchoalveolar lavage (BAL) was done 5 min and 48 h after challenge with saline or antigen. Airway cells were isolated and then stimulated ex vivo with a T-cell mitogen, phytohemagglutinin (PHA), and cytokine release was determined. Cells retrieved from the saline-challenged segment secreted principally interferon- γ (IFN- γ ) and IL-2. In contrast, cells obtained 48 h after allergen challenge secreted high levels of IL-5 and small but increased amounts of IL-4, IL-10, and granulocyte–macrophage colony-stimulating factor (GM-CSF). Although CD4⁺ T cells were a major source of IL-5, there were no significant changes in the relative proportion of CD4⁺ cells in response to bronchoprovocation. Additionally, ex vivo secretion of IL-5 by airway cells correlated closely with amounts of IL-5 and eosinophils present in the bronchoalveolar lavage fluid (BALF). These observations suggest that following exposure to allergen, airway T cells are functionally but not phenotypically different from resident airway T cells, and that T cells within the airway contribute to eosinophilic airway inflammation through the secretion of IL-5.