dc.contributor.author | Peña Asensio, Julia | |
dc.contributor.author | Calvo Sánchez, Henar | |
dc.contributor.author | Torralba González de Suso, Miguel | |
dc.contributor.author | Miquel Plaza, Joaquín | |
dc.contributor.author | Sanz de Villalobos, Eduardo | |
dc.contributor.author | Larrubia Marfil, Juan Ramón | |
dc.date.accessioned | 2022-03-07T10:18:42Z | |
dc.date.available | 2022-03-07T10:18:42Z | |
dc.date.issued | 2021-05-03 | |
dc.identifier.bibliographicCitation | Cells, 2021, v. 10, n. 3, p. 538- | en |
dc.identifier.issn | 2073-4409 | en |
dc.identifier.uri | http://hdl.handle.net/10017/50987 | |
dc.description.abstract | Hepatitis C virus (HCV)-specific CD8+ T cell response is essential in natural HCV infection control, but it becomes exhausted during persistent infection. Nowadays, chronic HCV infection can be resolved by direct acting anti-viral treatment, but there are still some non-responders that could benefit from CD8+ T cell response restoration. To become fully reactive, T cell needs the complete release of T cell receptor (TCR) signalling but, during exhaustion this is blocked by the PD-1 effect on CD28 triggering. The T cell pool sensitive to PD-1 modulation is the progenitor subset but not the terminally differentiated effector population. Nevertheless, the blockade of PD-1/PD-L1 checkpoint cannot be always enough to restore this pool. This is due to the HCV ability to impair other co-stimulatory mechanisms and metabolic pathways and to induce a pro-apoptotic state besides the TCR signalling impairment. In this sense, gamma-chain receptor cytokines involved in memory generation and maintenance, such as low-level IL-2, IL-7, IL-15, and IL-21, might carry out a positive effect on metabolic reprogramming, apoptosis blockade and restoration of co-stimulatory signalling. This review sheds light on the role of combinatory immunotherapeutic strategies to restore a reactive anti-HCV T cell response based on the mixture of PD-1 blocking plus IL-2/IL-7/IL-15/IL-21 treatment. | en |
dc.description.sponsorship | MINECO | es |
dc.description.sponsorship | Instituto de Salud Carlos III | es |
dc.description.sponsorship | European Commission | en |
dc.description.sponsorship | Gilead Fellowship Programme | en |
dc.description.sponsorship | European Regional Development Fund (ERDF) | en |
dc.format.mimetype | application/pdf | en |
dc.language.iso | eng | en |
dc.language.iso | eng | en |
dc.rights | © 2021 by the authors. Licensee MDPI | en |
dc.rights | Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) | en |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | en |
dc.subject | CD8+ T cell response | en |
dc.subject | Hepatitis C virus | en |
dc.subject | IL-15 | en |
dc.subject | IL-2 | en |
dc.subject | IL-21 | en |
dc.subject | IL-7 | en |
dc.subject | PD-1 | en |
dc.subject | PD-L1 | en |
dc.subject | Exhaustion | en |
dc.subject | Immune checkpoints | en |
dc.subject | Gamma-chain cytokines | en |
dc.title | Gamma-Chain Receptor Cytokines & PD-1 Manipulation to Restore HCV-Specific CD8 + T Cell Response during Chronic Hepatitis C | en |
dc.type | info:eu-repo/semantics/article | en |
dc.subject.eciencia | Medicina | es |
dc.subject.eciencia | Medicine | en |
dc.contributor.affiliation | Universidad de Alcalá. Departamento de Medicina y Especialidades Médicas | es |
dc.date.updated | 2022-03-07T10:15:59Z | |
dc.type.version | info:eu-repo/semantics/publishedVersion | en |
dc.identifier.doi | 10.3390/cells10030538 | |
dc.relation.projectID | info:eu-repo/grantAgreement/AEI/Plan Estatal de Investigación Científica y Técnica y de Innovación 2017-2020/ PI19%2F00206/ES/ | en |
dc.relation.projectID | info:eu-repo/grantAgreement/Gilead Sciences/ Gilead Fellowship Program in HIV & Hepatitis/ GLD14%2F00217 (JRL)/ES/ | en |
dc.relation.projectID | info:eu-repo/grantAgreement/Gilead Sciences/ Gilead Fellowship Program in HIV & Hepatitis/ GLD16%2F00014 (JRL)/ES/ | en |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | en |
dc.identifier.uxxi | AR/0000040468 | |
dc.identifier.publicationtitle | Cells | en |
dc.identifier.publicationvolume | 10 | |
dc.identifier.publicationissue | 3 | |
dc.identifier.publicationfirstpage | 538 | |