Allergic asthma is a complex syndrome characterized by airway obstruction, airway inflammation and airway hyper-responsiveness (AHR). Using a mouse model of allergen-induced AHR, we previously demonstrated that CD8-deficient mice develop significantly lower AHR, eosinophilic inflammation and interleukin (IL)-13 levels in bronchoalveolar lavage fluid compared with wild-type mice. These responses were restored by adoptive transfer of antigen-primed CD8⁺ T cells. Previously, two distinct populations of antigen-experienced CD8⁺ T cells, termed effector (T_EFF) and central memory (T_CM) cells, have been described^,,,. After adoptive transfer into CD8-deficient mice, T_EFF, but not T_CM, cells restored AHR, eosinophilic inflammation and IL-13 levels. T_EFF, but not T_CM, cells accumulated in the lungs, and intracellular cytokine staining showed that the transferred T_EFF cells were a source of IL-13. These data suggest an important role for effector CD8⁺ T cells in the development of AHR and airway inflammation, which may be associated with their Tc2-type cytokine production and their capacity to migrate into the lung.