First anti-HCV treatments, that include protease inhibitors in conjunction with IFN-α and Ribavirin, increase the sustained virological response (SVR) up to 80% in patients infected with HCV genotype 1. The effects of triple therapies on dendritic cell (DC) compartment have not been investigated. In this study we evaluated the effect of telaprevir-based triple therapy on DC phenotype and function, and their possible association with treatment outcome. HCV+ patients eligible for telaprevir-based therapy were enrolled, and circulating DC frequency, phenotype, and function were evaluated by flow-cytometry. The antiviral activity of plasmacytoid DC was also tested. In SVR patients, myeloid DC frequency transiently decreased, and returned to baseline level when telaprevir was stopped. Moreover, an up-regulation of CD80 and CD86 on mDC was observed in SVR patients as well as an improvement of IFN-α production by plasmacytoid DC, able to inhibit in vitro HCV replication. © 2017 Elsevier Inc.

Dendritic cells activation is associated with sustained virological response to telaprevir treatment of HCV-infected patients / Sacchi, A.; Tumino, N.; Turchi, F.; Refolo, G.; Fimia, G.; Ciccosanti, F.; Montalbano, M.; Lionetti, R.; Taibi, C.; D'Offizi, G.; Casetti, R.; Bordoni, V.; Cimini, E.; Martini, F.; Agrati, C.. - In: CLINICAL IMMUNOLOGY. - ISSN 1521-6616. - 183:(2017), pp. 82-90. [10.1016/j.clim.2017.07.017]

Dendritic cells activation is associated with sustained virological response to telaprevir treatment of HCV-infected patients

Fimia, G.;
2017

Abstract

First anti-HCV treatments, that include protease inhibitors in conjunction with IFN-α and Ribavirin, increase the sustained virological response (SVR) up to 80% in patients infected with HCV genotype 1. The effects of triple therapies on dendritic cell (DC) compartment have not been investigated. In this study we evaluated the effect of telaprevir-based triple therapy on DC phenotype and function, and their possible association with treatment outcome. HCV+ patients eligible for telaprevir-based therapy were enrolled, and circulating DC frequency, phenotype, and function were evaluated by flow-cytometry. The antiviral activity of plasmacytoid DC was also tested. In SVR patients, myeloid DC frequency transiently decreased, and returned to baseline level when telaprevir was stopped. Moreover, an up-regulation of CD80 and CD86 on mDC was observed in SVR patients as well as an improvement of IFN-α production by plasmacytoid DC, able to inhibit in vitro HCV replication. © 2017 Elsevier Inc.
2017
alpha interferon; B7 antigen; CD86 antigen; peginterferon alpha2a; ribavirin; telaprevir; alpha interferon; antivirus agent; B7 antigen; CD86 antigen; CD86 protein, human; macrogol derivative; oligopeptide; peginterferon alpha2a; recombinant protein; ribavirin; telaprevir, adult; aged; antiviral activity; Article; cell activation; cell function; clinical article; controlled study; cytokine production; dendritic cell; drug potentiation; female; flow cytometry; hepatitis C; Hepatitis C virus genotype 1; human; human cell; in vitro study; male; myeloid dendritic cell; phenotype; plasmacytoid dendritic cell; priority journal; T lymphocyte; treatment outcome; upregulation; virus replication; chronic hepatitis C; combination drug therapy; dendritic cell; immunology; middle aged; sustained virologic response, Aged; Antiviral Agents; B7-1 Antigen; B7-2 Antigen; Dendritic Cells; Drug Therapy, Combination; Female; Hepatitis C, Chronic; Humans; Interferon-alpha; Male; Middle Aged; Oligopeptides; Polyethylene Glycols; Recombinant Proteins; Ribavirin; Sustained Virologic Response; Treatment Outcome; Up-Regulation; Virus Replication; Dendritic cells; Directly acting antivirals; HCV; IFN-α; T cells
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Dendritic cells activation is associated with sustained virological response to telaprevir treatment of HCV-infected patients / Sacchi, A.; Tumino, N.; Turchi, F.; Refolo, G.; Fimia, G.; Ciccosanti, F.; Montalbano, M.; Lionetti, R.; Taibi, C.; D'Offizi, G.; Casetti, R.; Bordoni, V.; Cimini, E.; Martini, F.; Agrati, C.. - In: CLINICAL IMMUNOLOGY. - ISSN 1521-6616. - 183:(2017), pp. 82-90. [10.1016/j.clim.2017.07.017]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1411056
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