T-cell receptor recognizing Hepatitis B surface antigen-derived peptides presented by MHC class II (HBsAg-specific CD4+ TCR)

The T-cell receptor (TCR) on CD4+ T cells that recognizes Hepatitis B surface antigen (HBsAg) peptides presented by MHC class II molecules is a critical component of the adaptive immune response against the Hepatitis B virus (HBV) (Wisskirchen, K., et al., 2019, Journal of Hepatology). These TCRs enable CD4+ T cells to identify infected cells and provide essential help to B cells for antibody production and to CD8+ T cells for cytotoxic activity (Tan, A. T., et al., 2015, Journal of Clinical Investigation). In chronic HBV infection, these T-cell responses are often exhausted or deleted, leading to viral persistence and an increased risk of liver damage. Therapeutic strategies targeting or utilizing these TCRs include adoptive TCR-engineered T-cell therapy and therapeutic vaccines designed to restore or enhance the HBsAg-specific immune response (Gehring, A. J., et al., 2011, Gastroenterology). By specifically binding to HBsAg-MHC II complexes, these TCRs trigger the release of antiviral cytokines like interferon-gamma, which can inhibit viral replication and promote the clearance of infected hepatocytes. This target is particularly relevant for treating chronic hepatitis B and preventing the progression to hepatocellular carcinoma, as it addresses the underlying immune failure associated with the disease.

Other names

HBsAg-specific T-cell receptorHBV-specific CD4+ TCRMHC class II-restricted HBsAg TCRHepatitis B surface antigen-specific T-cell receptor

Recognition of HBsAg peptides on MHC class II molecules leads to CD4+ T-cell activation, secretion of antiviral cytokines (IFN-gamma, TNF-alpha), and orchestration of the broader immune response against HBV-infected hepatocytes (Boni, C., et al., 2007, Journal of Virology).