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Hepatitis B virus (HBV)-specific T-cell receptors (TCRs) are immune recognition complexes found on the surface of CD4+ and CD8+ T lymphocytes that specifically bind to HBV-derived peptides, such as those from the PreS2 and core proteins, presented by Human Leukocyte Antigen (HLA) molecules. These receptors are essential for the adaptive immune response against HBV; CD8+ T cells utilize them to identify and lyse infected hepatocytes, while CD4+ T cells provide critical cytokine support and direct antiviral effects. In chronic HBV infection and HBV-related hepatocellular carcinoma (HCC), these T-cell populations often become exhausted or deleted, leading to immune failure. Therapeutic strategies like TCR-engineered T-cell (TCR-T) therapy, including candidates such as SCG101 and LioCyx-M, involve the transfer of T cells equipped with high-affinity HBV-specific TCRs to restore viral clearance and target tumor cells. While promising, these therapies carry risks of significant hepatotoxicity due to the destruction of infected hepatocytes and require precise HLA matching for patient selection.
Adoptive cell transfer of T cells engineered with HBV-specific TCRs to recognize and eliminate HBV-infected or HBV-integrated cells via MHC-restricted antigen recognition; soluble TCR-bispecifics redirect endogenous T cells to target HBV-infected cells.
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