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Hepatitis B virus antigen-MHC complexes are molecular structures formed by the presentation of HBV-derived peptide fragments bound to major histocompatibility complex (MHC) molecules on the surface of infected cells or professional antigen-presenting cells. MHC class I complexes present HBV peptides from internalized or synthesized viral proteins to CD8+ cytotoxic T cells, mediating the immune recognition and destruction of infected hepatocytes[1][2][6]. MHC class II complexes present HBV peptides primarily from endocytosed viral material to CD4+ helper T cells, orchestrating broader immune responses[1]. These complexes play a central role in both antiviral immunity (leading to viral clearance) and the immunopathogenesis of hepatitis B, with their efficacy and regulation influencing the outcome of infection—ranging from viral clearance to chronic infection and liver damage. They are therapeutic targets for novel immunotherapies (such as TCR-mimic antibodies) and are involved in mechanisms underlying both protective immunity and liver immunopathology in HBV infection[1][2][6].
Recognition and killing of infected hepatocytes by CD8+ cytotoxic T lymphocytes, following presentation of HBV-derived peptides by MHC class I complexes[1][2][6] Activation of CD4+ T helper cells via MHC class II complexes with HBV peptides on antigen-presenting cells (APCs)[1]
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