Innate signaling regulates cross-priming at the level of DC licensing and not antigen presentation.
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.
Keller
Susanne A
SA
Cytos Biotechnology AG, Schlieren, Switzerland.
Schwarz
Katrin
K
Manolova
Vania
V
von Allmen
Caroline E
CE
Kinzler
Matthias G
MG
Bauer
Monika
M
Muntwiler
Simone
S
Saudan
Philippe
P
Bachmann
Martin F
MF
D000818:Animals; D017951:Antigen Presentation; D045142:Cross-Priming; D003713:Dendritic Cells / Q000276:immunology* / Q000378:metabolism; D007113:Immunity, Innate; D008217:Lymphocytic choriomeningitis virus / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D008854:Microscopy, Electron; D015398:Signal Transduction; D051193:Toll-Like Receptors / Q000276:immunology / Q000378:metabolism; D014764:Viral Proteins / Q000276:immunology; D014771:Virion / Q000276:immunology / Q000648:ultrastructure
D051193:Toll-Like Receptors; D014764:Viral Proteins