Listeria-infected myeloid dendritic cells produce IFN-beta, priming T cell activation
Autor: | Pengcheng Zhu, Judy Lieberman, Hanping Feng, Shenghe Cai, Ann Schlesinger, Laura E. Maliszewski, Dong Zhang, Deborah Palliser |
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Rok vydání: | 2005 |
Předmět: |
Antigens
Differentiation T-Lymphocyte Myeloid Hot Temperature CD3 Complex T cell T-Lymphocytes Immunology Receptors Antigen T-Cell Priming (immunology) In Vitro Techniques medicine.disease_cause Lymphocyte Activation Mice Listeria monocytogenes Antigens CD medicine Immunology and Allergy Animals Secretion Lectins C-Type Myeloid Cells RNA Messenger Mice Knockout Mice Inbred BALB C biology CD69 T-cell receptor Dendritic Cells Interferon-beta biology.organism_classification Cell biology Mice Inbred C57BL medicine.anatomical_structure Mutation Listeria |
Zdroj: | Journal of immunology (Baltimore, Md. : 1950). 175(1) |
ISSN: | 0022-1767 |
Popis: | 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-β, which requires bacterial cytosolic invasion. Exposure to high concentrations of IFN-β sensitizes naive T cells for Ag-dependent activation. |
Databáze: | OpenAIRE |
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