Ramos, ManuelGarcia-Barreno, BlancaLopez, DanielMelero, Jose AntonioVal, Margarita delJohnstone, Carolina2020-07-022020-07-022012-11Immunol Cell Biol . 2012 Nov;90(10):978-82.0818-9641http://hdl.handle.net/20.500.12105/10633Respiratory syncytial virus causes lower respiratory tract infections in infancy and old age, affecting also immunocompromised patients. The viral fusion protein is an important vaccine candidate eliciting antibody and cell-mediated immune responses. CD8(+) cytotoxic T lymphocytes (CTLs) are known to have a role in both lung pathology and viral clearance. In BALB/c mice, the fusion protein epitope F249-258 is presented to CTLs by the murine major histocompatibility complex (MHC) class I molecule K(d). In cells infected with recombinant vaccinia viruses encoding the fusion protein, F249-258 is presented by MHC class I molecules through pathways that are independent of the transporters associated with antigen processing (TAP). We have now found that F249-258 can be generated from non-infectious virus from an exogenous source. Antigen processing follows a lysosomal pathway that appears to require autophagy. As a practical consequence, inactivated virus suffices for in vivo priming of virus-specific CTLs.engAMAntigen PresentationAgedAnimalsAntigens, LyAntigens, ViralAutophagyCell LineEpitopes, T-LymphocyteHistocompatibility Antigens Class IHumansImmunocompromised HostInfantLysosomesMembrane ProteinsMiceMice, Inbred BALB CPeptide FragmentsRecombinant Fusion ProteinsRespiratory Syncytial Virus InfectionsRespiratory Syncytial VirusesT-Lymphocytes, CytotoxicViral VaccinesExogenous, TAP-independent lysosomal presentation of a respiratory syncytial virus CTL epitope.AtribuciĆ³n-NoComercial-CompartirIgual 4.0 Internacional229291809010978-8210.1038/icb.2012.431440-1711Immunology and cell biologyopen access