Innate signaling regulates cross‐priming at the level of DC licensing and not antigen presentation

AbstractInnate 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‐α/β 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.