Listeria-infected myeloid dendritic cells produce IFN-beta, priming T cell activation.


The intracellular bacterium Listeria monocytogenes infects dendritic cells (DC) and other APCs and induces potent cell-mediated protective immunity. However, heat-killed bacteria fail to do so. This study explored whether DC differentially respond to live and killed Listeria and how this affects T cell activation. To control for bacterial number, a replication-deficient strain, Lmdd, defective in D-alanine biosynthesis, was used. We found that DC internalize both live and heat-killed Lmdd and similarly up-regulate the expression of costimulatory molecules, a necessary step for T cell activation. However, only live Lmdd-infected DC stimulate T cells to express the early activation marker CD69 and enhance T cell activation upon TCR engagement. Infection with live, but not heat-killed, Lmdd induces myeloid DC to secrete copious amounts of IFN-beta, which requires bacterial cytosolic invasion. Exposure to high concentrations of IFN-beta sensitizes naive T cells for Ag-dependent activation.

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@article{Feng2005ListeriainfectedMD, title={Listeria-infected myeloid dendritic cells produce IFN-beta, priming T cell activation.}, author={Hanping Feng and Dong Zhang and Deborah Palliser and Pengcheng Zhu and Shenghe Cai and Ann Schlesinger and Laura E Maliszewski and Judy Lieberman}, journal={Journal of immunology}, year={2005}, volume={175 1}, pages={421-32} }