Fig. 11.

Schema of the possible mechanism of ethanol metabolism/acetaldehyde (Ach) affects presentation of hepatitis B virus (HBV)-peptide-major histocompatibility complex I (MHC class I) [cytotoxic T lymphocyte (CTL) epitopes] on the surface of hepatocytes, which are targets for immune response. Although Ach increases HBV replication, it directly suppresses processing of HBV peptides by proteasome and indirectly affects immunoproteasome function and induction of peptide-loading complex components tapasin and transporter associated with antigen processing 1 (TAP1), by impairing interferon-γ (IFNγ) signaling in hepatocytes. Finally, Ach suppresses presentation of HBV peptide-MHC class I complexes on the surface of hepatocytes, which may lower activation of CTLs (achieved by interaction of T cell receptor on CD8⁺ T lymphocytes with HBV peptide-MHC class I complex on hepatocytes) and ability of CTLs to recognize HBV-expressing hepatocytes as a target. ER, endoplasmic reticulum.