Legionella pneumophila, the aetiologic agent of Legionnaires’ disease is an opportunistic, intracellular bacterium that causes a severe pneumonia of the lung in immunocompromised individuals. Though extensively studied, the molecular and cellular immune mechanisms controlling bacterial replication in mammalian hosts remain poorly understood. We demonstrated that plasmacytoid dendritic cells (pDCs) were recruited into the lung of L. pneumophila-infected mice within 24 hours of infection. In vivo depletion of pDCs from L. pneumophila-infected mice resulted in an increase in bacterial load by 72 hours, and their mechanism of action was independent of type-I interferon, a class of antiviral cytokines predominantly secreted by these cells1. Here, we report that pDC recruitment peaked at 72 hours after infection and involved an 11-fold increase in pDCs coexpressing the alpha- and beta-chain isoforms of CD8. Aside from type-I interferon, pDCs also secrete other proinflammatory cytokines, including IL-12 and IL-18. We identified that IL-12p40, but not IL-18 was important in immune clearance of L. pneumophila. To investigate the relationship between IL-12p40 and pDC activity, we developed a pDC adoptive transfer model. Transfer of wild-type pDCs into the lung during L. pneumophila infection significantly reduced bacterial load within 48 hours, relative to mice that did not receive pDCs. Subsequent supplementation of wild-type, IL-12p40-sufficient pDCs into the lungs of L. pneumophila-infected IL-12p40-deficient mice revealed a restoration of bacterial clearance, as mice receiving IL-12p40-deficient pDCs contained a significantly higher bacterial load in the lung. This indicated a role of IL-12p40 in an innate immune function of pDCs against L. pneumophila.