Authors:
Brian T. Edelson, Tara R. Bradstreet, Kai Hildner, Javier A. Carrero, Katherine E. Frederick, Wumesh KC, Roger Belizaire, Taiki Aoshi, Robert D. Schreiber, Mark J. Miller, Theresa L. Murphy, Emil R. Unanue, & Kenneth M. Murphy
Summary:
CD8α+ dendritic cells (DCs) prime cytotoxic T lymphocytes during viral infections and produce interleukin-12 in response to pathogens. Although the loss of CD8α+ DCs in Batf3/ mice increases their susceptibility to several pathogens, we observed that Batf3/ mice exhibited enhanced resistance to the intracellular bacterium Listeria monocytogenes. In wild-type mice, Listeria organisms, initially located in the splenic marginal zone, migrated to the periarteriolar lymphoid sheath (PALS) where they grew exponentially and induced widespread lymphocyte apoptosis. In Batf3/ mice, however, Listeria organisms remain trapped in the marginal zone, failed to traffic into the PALS, and were rapidly cleared by phagocytes. In addition, Batf3/ mice, which lacked the normal population of hepatic CD103+ peripheral DCs, also showed protection from liver infection. These results suggest that Batf3-dependent CD8α+ and CD103+ DCs provide initial cellular entry points within the reticuloendothelial system by which Listeria establishes productive infection.
Source:
Immunity; Vol. 35, Issue 2, 236-248 (08/26/11)