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...

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Main Authors: Keller, SA, Schwarz, K, Manolova, V, von Allmen, C, Kinzler, MG, Bauer, M, Muntwiler, S, Saudan, P, Bachmann, M
Format: Journal article
Language:English
Published: 2010
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author Keller, SA
Schwarz, K
Manolova, V
von Allmen, C
Kinzler, MG
Bauer, M
Muntwiler, S
Saudan, P
Bachmann, M
author_facet Keller, SA
Schwarz, K
Manolova, V
von Allmen, C
Kinzler, MG
Bauer, M
Muntwiler, S
Saudan, P
Bachmann, M
author_sort Keller, SA
collection OXFORD
description 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.
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spelling oxford-uuid:7b32f46b-82a5-41c0-bbd5-d1aca11c79f62022-03-26T20:49:05ZInnate signaling regulates cross-priming at the level of DC licensing and not antigen presentation.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:7b32f46b-82a5-41c0-bbd5-d1aca11c79f6EnglishSymplectic Elements at Oxford2010Keller, SASchwarz, KManolova, Vvon Allmen, CKinzler, MGBauer, MMuntwiler, SSaudan, PBachmann, MInnate 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.
spellingShingle Keller, SA
Schwarz, K
Manolova, V
von Allmen, C
Kinzler, MG
Bauer, M
Muntwiler, S
Saudan, P
Bachmann, M
Innate signaling regulates cross-priming at the level of DC licensing and not antigen presentation.
title Innate signaling regulates cross-priming at the level of DC licensing and not antigen presentation.
title_full Innate signaling regulates cross-priming at the level of DC licensing and not antigen presentation.
title_fullStr Innate signaling regulates cross-priming at the level of DC licensing and not antigen presentation.
title_full_unstemmed Innate signaling regulates cross-priming at the level of DC licensing and not antigen presentation.
title_short Innate signaling regulates cross-priming at the level of DC licensing and not antigen presentation.
title_sort innate signaling regulates cross priming at the level of dc licensing and not antigen presentation
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