Hepatitis B or C virus (HBV or HCV) causes chronic liver diseases that eventually progress to liver cancer. Both viruses are armed with multiple machineries for modulating immune responses in infected hosts. Mild and pervasive immune cell dysfunction, but not fully compromised, is a hallmark of chronic HBV or HCV infection, of which fundamental mechanisms are yet to be clarified. Dendritic cells (DC) as immune sentinels sense virus via toll-like receptors (TLR) or retinoic acid inducible gene-I (RIG-I) and evoke a cascade of immune reactions by secreting cytokines or by interacting other lymphocytes. Reduced and disabled DC potentially give negative impact on adjacent cells, such as NK cells, NKT cells and T cells. However, lack of evidence for active viral replication in DC or blood cells imply the presence of undisclosed contrivances that are independent of infection. Successful treatment of chronically infected patients with anti-viral agents is accompanied with numerical and/or functional restoration of DC, suggesting that DC could serve as potential therapeutic targets. Further studies are warranted for the establishment of therapeutic DC vaccine in order to gain more vigorous and sustained virus-specific immune responses. Cross talk between DC and lymphocytes are thus critical in shaping innate and subsequent adaptive immune responses against hepatitis virus, either spontaneously or therapeutically.
Keywords: Dendritic cells, HBV, HCV, interferon, natural killer cells, natural killer T cells, T cells, therapeutic DC vaccine, hepatitis virus, anti-viral therapy
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