AbstractThe biology of the eosinophilic leukocyte—development, recruitment, and prolonged existence in somatic tissues—has been linked almost invariably to the actions of the “eosinophil” cytokine, interleukin-5 (IL-5). Here we demonstrate that pulmonary eosinophilia can occur in the absence of IL-5, as morphologically normal eosinophils are recruited to the lungs of virus-infected IL-5 −/− mice with kinetics and sequelae that are indistinguishable from those of their IL-5 +/+ counterparts. We conclude that pulmonary eosinophilia observed in response to primary paramyxovirus infection occurs via mechanisms that are distinct from those involved in eosinophil responses to allergens and in asthma. Furthermore, the presence of functional eosinophils in IL-5 −/− mice suggests the possibility of developmentally distinct subsets of what has been presumed to be a homogeneous leukocyte population.