Effector CD8+ T cells mediate inflammation and airway hyper-responsiveness

Allergic asthma is a complex syndrome characterized by airway obstruction, airway inflammation and airway hyperresponsiveness (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(1). Previously, two distinct populations of antigen-experienced CD8(+) T cells, termed effector (T-EFF) and central memory (T-CM) cells, have been described(2-5). 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.