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Innate stimuli, such as TLR ligands, are known to greatly facilitate cross-priming. Currently it is unclear whether innate stimuli enhance cross-priming at the level of cross-presentation or at the level of T-cell priming. In this study, we addressed this question by measuring cross-presentation as well as cross-priming by virus-like particles (VLP) displaying peptide p33 derived of lymphocytic choriomeningitis virus. Innate stimuli were varied by either packaging different TLR ligands into virus-like particles or using mice deficient in two key molecules of TLR-signaling, namely the adaptor molecule MyD88 as well as IFN-alpha/beta receptor. While efficient cross-presentation occurred despite strongly reduced activation of DC in the absence of TLR ligand-mediated signals, T-cell priming was abolished. Thus, innate stimuli regulate cross-priming at the level of DC licensing for T-cell activation and not antigen presentation.

Original publication




Journal article


Eur J Immunol

Publication Date





103 - 112


Animals, Antigen Presentation, Cross-Priming, Dendritic Cells, Immunity, Innate, Lymphocytic choriomeningitis virus, Mice, Mice, Inbred C57BL, Microscopy, Electron, Signal Transduction, Toll-Like Receptors, Viral Proteins, Virion