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Immunotherapy with interferon-α-induced dendritic cells for chronic HCV infection (the results of pilot clinical trial).

Immunotherapy with interferon-α-induced dendritic cells for chronic HCV infection (the results of pilot clinical trial).
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Chernykh E, Leplina O, Oleynik E, Tikhonova M, Tyrinova T, Starostina N, Ostanin A,


Chernykh E, Leplina O, Oleynik E, Tikhonova M, Tyrinova T, Starostina N, Ostanin A, (click to view)

Chernykh E, Leplina O, Oleynik E, Tikhonova M, Tyrinova T, Starostina N, Ostanin A,

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Immunologic research 2017 11 21() doi 10.1007/s12026-017-8967-2

Abstract

The key role of T cells in hepatitis C virus (HCV) elimination and the ability of dendritic cells (DCs) to induce antiviral T cell responses suggest that DC vaccines could be a promising approach in the treatment of chronic HCV infection. The aim of our study was to evaluate, whether immunotherapy with DCs is safe and elicits anti-HCV T cell responses. Ten patients with HCV (genotype 1) were vaccinated with monocyte-derived DCs, generated in the presence of IFN-α (IFN-DCs) and pulsed with recombinant HCV Core and NS3 proteins. Treatment schedule included four subcutaneous vaccinations with 1 week interval and six vaccinations with month interval. No serious adverse events or an increase in hepatitis C biochemical activity were registered after vaccination. Using ex vivo assays for the detection of proliferative responses, IFN-γ production and CD8(+) degranulation have shown that immunotherapy elicited antigen-specific responses in all patients although individual heterogeneity existed within their types, magnitude, and timing. Core/NS3-specific proliferative response and CD8(+) T cell degranulation have already been registered after the first course of vaccination. Of note, Core-specific responses had higher magnitude. The appearance of antigen-specific IFN-γ responses was registered after the second vaccination course. Vaccination did not cause Th2 response and expansion of the CD4(+)CD25(+)CD127(-) regulatory T cells. Generated immune responses failed to provide virus elimination. Nevertheless, there were inverse correlations between viral load and NS3-specific proliferation (R S = 0.62; p = 0.05) and IFN-γ secretion (R S = - 0.82; p = 0.001) at 6-month post-treatment period. Immunotherapy with IFN-DCs was safe and elicited HCV-specific T cell responses which were insufficient to eliminate viruses but could be implicated in the restriction of viral replication.

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