Journal
IMMUNITY
Volume 35, Issue 2, Pages 236-248Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2011.06.012
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Funding
- Howard Hughes Medical Institute
- Burroughs Wellcome Fund Career Award for Medical Scientists
- Washington University School of Medicine
- German Research Foundation
- National Institutes of Health
- Grants-in-Aid for Scientific Research [22790461] Funding Source: KAKEN
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CD8 alpha(+) dendritic cells (DCs) prime cytotoxic T lymphocytes during viral infections and produce interleukin-12 in response to pathogens. Although the loss of CD8 alpha(+) 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 CD8 alpha(+) and CD103(+) DCs provide initial cellular entry points within the reticuloendothelial system by which Listeria establishes productive infection.
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