Hepatitis B virus surface antigen-specific B-cell receptors and T-cell receptors (HBsAg-specific BCR/TCR)

Hepatitis B virus surface antigen-specific B-cell receptors (BCRs) and T-cell receptors (TCRs) are the primary mediators of the adaptive immune response against the Hepatitis B virus (HBV) (Bertoletti & Ferrari, 2016). BCRs on B cells recognize the surface antigen (HBsAg) to produce neutralizing antibodies, while TCRs on T cells recognize HBsAg-derived peptides presented by Major Histocompatibility Complex (MHC) molecules on the surface of infected hepatocytes (Gehring & Protzer, 2019). In chronic HBV infection, these immune cells often become dysfunctional or exhausted, failing to clear the virus and allowing for persistent infection and potential progression to hepatocellular carcinoma (HCC) (Tan et al., 2021). Modern therapeutic strategies, such as adoptive T-cell therapy (TCR-T) and chimeric antigen receptor (CAR-T) therapy, involve engineering a patient's immune cells to express high-affinity HBsAg-specific receptors to bypass natural immune exhaustion (Tan et al., 2021). Additionally, therapeutic vaccines like VTP-300 and BRII-179 are designed to reinvigorate or induce these specific BCR and TCR populations to achieve a functional cure, defined by the loss of HBsAg and the development of protective immunity (Gehring & Protzer, 2019).

Other names

HBsAg-specific BCRHBsAg-specific TCRAnti-HBs BCRAnti-HBs TCRHBV-specific immune receptorsHepatitis B surface antigen-specific immune receptors

Adoptive transfer of T cells engineered with HBsAg-specific receptors to recognize and lyse infected hepatocytes or HBV-related tumor cells; induction of endogenous HBsAg-specific immune responses via therapeutic vaccination to achieve viral clearance.