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dc.contributor.authorJohnstone, Carolina-
dc.contributor.authorRamos, Manuel-
dc.contributor.authorLópez, Daniel-
dc.contributor.authorMelero, José A.-
dc.contributor.authorGarcía-Barreno, Blanca-
dc.contributor.authorVal, Margarita del-
dc.identifierdoi: 10.1038/icb.2012.43-
dc.identifierissn: 0818-9641-
dc.identifier.citationImmunology and Cell Biology 90: 978- 982 (2012)-
dc.description.abstractRespiratory 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 Kd. 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.-
dc.publisherBlackwell Publishing-
dc.titleExogenous, TAP-independent lysosomal presentation of a respiratory syncytial virus CTL epitope-
dc.description.versionPeer Reviewed-
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