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Bloodstream infections induce considerable morbidity, high mortality, and represent a significant burden of cost in health care; however, our understanding of the immune response to bacteremia is incomplete. Langerin +  CD8α +  dendritic cells (DCs), residing in the marginal zone of the murine spleen, have the capacity to cross-prime CD8 +  T cells and produce IL-12, both of which are important components of antimicrobial immunity. Accordingly, we hypothesized that this DC subset may be a key promoter of adaptive immune responses to blood-borne bacterial infections. Utilizing mice that express the diphtheria toxin receptor under control of the langerin promoter, we investigated the impact of depleting langerin +  CD8α +  DCs in a murine model of intravenous infection with  Mycobacterium bovis  bacille Calmette–Guerin (BCG). In the absence of langerin +  CD8α +  DCs, the immune response to blood-borne BCG infection was diminished: bacterial numbers in the spleen increased, serum IL-12p40 decreased, and delayed CD8 +  T cell activation, proliferation, and IFN-γ production was evident. Our data revealed that langerin +  CD8α +  DCs play a pivotal role in initiating CD8 +  T cell responses and IL-12 production in response to bacteremia and may influence the early control of systemic bacterial infections.

Langerin+ CD8α+ Dendritic Cells Drive Early CD8+ T Cell Activation and IL-12 Production During Systemic Bacterial Infection