Despite initially encouraging data from preclinical and clinical studies, the efficacy of human adenoviral vector serotype

5 (AdHu5) was hampered by a strong pre-existing anti-vector immunity among vaccinated macaques, in which transgene-specific T cells homed to different organs in the presence of anti-vector immunity.140Listeria monocytogenes is known to induce strong cellular immune responses. Listeria monocytogenes induces multiple effector mechanisms, including antigen presentation via MHC class I and II pathways as well as induction of innate immune responses.141 As L. monocytogenes is a ubiquitous bacterium, anti- L. monocytogenes immune responses are likely to be selleckchem present among the majority of individuals. Sciaranghella et al.142 constructed a live-attenuated L. monocytogenes learn more vector, which encodes SIVmac239 gag. The novel, live-attenuated L. monocytogenes vector may be an attractive

platform for oral vaccine delivery. Although HCV leads to impairment of both MDC and PDC according to many researchers, the mechanisms how HCV affects DC function remains elusive.55 Further research is needed in regard to the mechanisms of HCV-induced DC impairment and the correlation between DC function and HCV persistence. Dendritic cell-based vaccination/therapeutic approaches are safe and promising in terms of their propensity to establish anti-HCV adaptive immune responses. However, possible side-effects of DC-based therapeutic vaccine should be carefully evaluated, especially those possibly inducing

a strong T-cell-mediated immunity, because of the dual role of virus-specific cytotoxic T cells mediating both viral clearance and tissue Cyclin-dependent kinase 3 damage. Nevertheless, the achievements in this field of studies brought us the hope of opening new routes to the prevention and treatment of HCV infection. Prospects of a DC-based vaccine against HCV infection include employment of adjuvants, the blockage of negative regulatory signal and enhancement of positive regulatory signals, so as to improve the vaccine immune response against HCV infection, reduce HCV viral load, and hinder progression of chronic liver disease. This work is supported by the National High Technology Research and Development Program of China (No. 2007AA02Z441, 863 Program) and the National Natural Science Foundation of China (No.31170877 and No.81170389). No conflicting financial interests exist. “
“IL-17-producing CD4+ T cells (Th17) have been classified as a new T helper cell subset. Using an IL-17 fate mapping mouse strain, which genetically fixes the memory of IL-17 expression, we demonstrate that IL-17A/F-expressing T helper cells generated either in vitro or in vivo are not a stable T-cell subset. Upon adoptive transfer of IL-17F-reporter-positive Th17 cells to RAG-deficient or WT animals, encephalitogenic Th17 cells partially lose IL-17 expression and upregulate IFN-γ.