Although activated CD4⁺ T cells have been implicated in the pathogenesis of asthma, the direct contribution of this leukocyte to the induction of aeroallergen-induced bronchial hyperreactivity and lung damage is unknown. In the present investigation, we have used a model of allergic airways inflammation, which displays certain phenotypic characteristics of late-phase asthmatic responses, together with interleukin-5–deficient (IL-5^{− / −}) mice and donor antigen–specific CD4⁺ TH2-type cells to obtain unequivocal evidence for a role of this T lymphocyte in the pathophysiology of allergic airways inflammation. Antigen-primed CD4⁺ T cells and CD4⁻ cells (CD4⁺-depleted population) were purified from the spleens of ovalbumin (OVA)-sensitized wild-type mice and adoptively transferred to OVA-sensitized and nonsensitized IL-5^{− / −} mice. In vitro stimulation of the purified cell populations with OVA resulted in the secretion of IL-4 and IL-5, but not interferon- γ , from the CD4⁺ T cells, indicating that they were of the TH2 type. In contrast, interferon- γ , but not IL-4 and IL-5, was produced by the CD4⁻ T cells. The CD4⁺ TH2-type cells (but not the CD4⁻ cells) reconstituted aeroallergen (OVA)-induced blood and airways eosinophilia, lung damage, and airways hyperreactivity to β -methacholine in IL-5^{− / −} mice. The reconstitution did not require prior sensitization of the mice, but it did not occur if they were aerosolized with saline instead of OVA. The circulating levels of OVA-specific -IgE and -IgG₁ were not significantly altered by the adoptive transfer of either cell population. These investigations establish that IL-5–secreting CD4⁺ TH2-type cells play a pivotal role in generating blood and airways eosinophilia and in the subsequent development of bronchial hyperreactivity and lung damage that occurs in response to aeroallergens.