| Literature DB >> 21867927 |
Brian T Edelson1, 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.
Abstract
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.Entities:
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Year: 2011 PMID: 21867927 PMCID: PMC3172670 DOI: 10.1016/j.immuni.2011.06.012
Source DB: PubMed Journal: Immunity ISSN: 1074-7613 Impact factor: 31.745