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The Hepatitis B virus-specific T-cell receptor (HBV-specific TCR) is a specialized heterodimeric surface protein on T lymphocytes that recognizes HBV-derived peptides presented by Major Histocompatibility Complex (MHC) molecules (Wisskirchen et al., 2019). These receptors are the primary mediators of the adaptive immune response against HBV, enabling CD8+ T cells to lyse infected hepatocytes and CD4+ T cells to coordinate the broader immune response (Tan et al., 2019). In chronic HBV infection, the endogenous HBV-specific T-cell population often becomes functionally exhausted or deleted, which prevents viral clearance and increases the risk of progression to hepatocellular carcinoma (HCC) (Boni et al., 2007). Therapeutic strategies such as TCR-engineered T-cell (TCR-T) therapy involve the ex vivo modification of a patient's T cells to express high-affinity TCRs specific to HBV antigens like HBsAg, HBcAg, or HBx (Lion TCR, 2024). These engineered cells are designed to target and eliminate both HBV-infected cells and HBV-DNA integrated tumor cells, offering a potential functional cure for chronic hepatitis B and a novel treatment for HBV-associated liver cancer (SCG Cell Therapy, 2024).
Adoptive cell therapy involving the engineering of T cells to express specific T-cell receptors (TCRs) that recognize Hepatitis B virus (HBV) antigens (such as HBsAg or HBcAg) presented by Major Histocompatibility Complex (MHC) molecules, leading to the targeted destruction of HBV-infected hepatocytes or HBV-related tumor cells (Wisskirchen et al., 2019).
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