Figure 2

Selective TLR 7 agonists in chronic viral hepatitis. Selective oral TLR7 agonists are absorbed through the gastrointestinal mucosa and enter the liver through portal circulation (A). In the liver, they lead to priming of immature DCs to mature DC secreting interferon-α. Interferon-α stimulation will lead to the synthesis of interferon-stimulated gene (ISG) products, which in turn facilitate suppression of hepatitis viral replication (green insert) (B). Although, the exact mechanism of how interferon-α suppresses hepatitis replication is not fully characterized, multiple stages of hepatitis replication (such as viral entry, transcription, translation and assembly) have been shown to be inhibited by interferon-α and ISGs. In the lymphatics, TLR7 stimulated mature DCs secrete IL-12 and preferentially activate T cells to differentiate into T_H1 cells (C). A T_H1 response leads to the generation of cytotoxic T cell response (red inserts). IFN-γ primed CTLs cause suppression of hepatitis viruses by either killing infected hepatocyte or by shutting down the virion assembly.