2026-06-14T03:40:11Zhttps://repisalud.isciii.es/rest/oai/request

oai:repisalud.isciii.es:20.500.12105/106332024-09-27T23:01:32Zcom_20.500.12105_2052com_20.500.12105_2051col_20.500.12105_19609

00925njm 22002777a 4500 dc Ramos, Manuel author Garcia-Barreno, Blanca author Lopez, Daniel author Melero, Jose Antonio author Val, Margarita del author Johnstone, Carolina author 2012-11 Respiratory 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. Immunol Cell Biol . 2012 Nov;90(10):978-82. 10.1038/icb.2012.43 1440-1711 0818-9641 Immunology and cell biology 22929180 http://hdl.handle.net/20.500.12105/10633 Exogenous, TAP-independent lysosomal presentation of a respiratory syncytial virus CTL epitope.