| First Author | Keller SA | Year | 2010 |
| Journal | Eur J Immunol | Volume | 40 |
| Issue | 1 | Pages | 103-12 |
| PubMed ID | 19877013 | Mgi Jnum | J:155695 |
| Mgi Id | MGI:4415105 | Doi | 10.1002/eji.200939559 |
| Citation | Keller SA, et al. (2010) Innate signaling regulates cross-priming at the level of DC licensing and not antigen presentation. Eur J Immunol 40(1):103-12 |
| abstractText | 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. |
