Hepatitis B surface antigen-specific immune receptor

Hepatitis B surface antigen-specific immune receptors are a class of recognition proteins, including T-cell receptors (TCRs), chimeric antigen receptors (CARs), and B-cell receptors (BCRs), that specifically bind to the Hepatitis B surface antigen (HBsAg) (1, 2). These receptors are fundamental to the adaptive immune response against the Hepatitis B virus (HBV), enabling the identification and destruction of infected hepatocytes and HBV-related tumor cells (3, 5). In chronic HBV infection, endogenous HBsAg-specific receptors often become dysfunctional or exhausted due to prolonged antigen exposure and high viral loads, leading to viral persistence and an increased risk of hepatocellular carcinoma (HCC) (6, 10). Therapeutically, these receptors are utilized as engineered components of adoptive cell therapies or as targets for immune restoration strategies (4, 7). Engineered TCR-T and CAR-T cells, such as SCG101, utilize high-affinity HBsAg-specific receptors to bypass natural immune tolerance and directly eliminate infected cells (4, 5). Conversely, therapeutic vaccines and checkpoint inhibitors aim to revitalize endogenous HBsAg-specific receptors to achieve a functional cure, characterized by sustained HBsAg loss (8, 12). Clinical application of these therapies requires careful management of safety concerns, particularly liver inflammation (ALT flares) and cytokine release syndrome, which can result from the rapid destruction of infected liver tissue (1, 4).

Other names

HBsAg-specific T-cell receptorHBsAg-specific chimeric antigen receptorHBsAg-specific B-cell receptorHBV-specific immune receptorAnti-HBs receptor

Adoptive cell therapy (redirecting T cells via engineered receptors), immune checkpoint inhibition (reversing exhaustion of endogenous receptors), and active immunization (stimulating endogenous receptor expansion).