An autologous, mRNA-engineered TCR-T cell therapy in which a patient’s T cells are transiently redirected to express HBV antigen–specific T-cell receptors that recognize HBV-derived peptides presented by HLA-A*02:01 or HLA-A*24:02 on tumor cells, inducing TCR/MHC class I–dependent activation and cytotoxic killing of HBV-related hepatocellular carcinoma; administered IV weekly at 5–10×10^6 cells/kg.
Autologous T cells are mRNA-engineered to transiently express HBV-specific T-cell receptors that recognize HBV-derived peptides presented by HLA-A*02:01 or HLA-A*24:02 on tumor cells, triggering TCR/MHC class I–dependent activation and cytotoxic killing of HBV-related hepatocellular carcinoma cells.
YES
DIRECT
Engineered TCR-T cells recognize HBV peptide–HLA-A*02:01 complexes on tumor cells, become activated, and kill them via cytotoxic T-cell effector mechanisms (perforin/granzyme release and Fas–FasL–mediated apoptosis).
An autologous, mRNA-engineered TCR-T cell therapy in which a patient’s T cells are transiently redirected to express HBV antigen–specific T-cell receptors that recognize HBV-derived peptides presented by HLA-A*02:01 or HLA-A*24:02 on tumor cells, inducing TCR/MHC class I–dependent activation and cytotoxic killing of HBV-related hepatocellular carcinoma; administered IV weekly at 5–10×10^6 cells/kg.
Autologous T cells are mRNA-engineered to transiently express HBV-specific T-cell receptors that recognize HBV-derived peptides presented by HLA-A*02:01 or HLA-A*24:02 on tumor cells, triggering TCR/MHC class I–dependent activation and cytotoxic killing of HBV-related hepatocellular carcinoma cells.
YES
DIRECT
mRNA-engineered TCR-T cells recognize the HBV-derived peptide–HLA-A*24:02 complex via their TCR, activating cytotoxic T-cell effector functions that kill target cells through perforin/granzyme release and Fas–FasL–mediated apoptosis.
Autologous TCR-T cells engineered via mRNA to transiently express HBV antigen–specific T-cell receptors that recognize HBV peptides presented by HLA-A*02:01 or HLA-A*24:02 on tumor cells, driving TCR/MHC class I–dependent activation and cytotoxicity against HBV-related hepatocellular carcinoma; administered by weekly IV infusion at 5–10×10^6 cells/kg.
Autologous T cells are transiently mRNA-engineered to express HBV-specific T-cell receptors that recognize HBV-derived peptides presented by HLA-A*02:01 or HLA-A*24:02 on tumor cells, triggering TCR/MHC class I–dependent activation and cytotoxic killing of HBV-related hepatocellular carcinoma cells.
YES
DIRECT
Engineered TCR-T cells recognize the HLA-A*02:01–HBV peptide complex on tumor cells and induce TCR/MHC I–dependent killing via perforin/granzyme release and Fas–FasL–mediated apoptosis.
Autologous cellular immunotherapy in which patient-derived dendritic cells are pulsed with tumor-specific neoantigen peptides to present via HLA class I/II and prime/expand neoantigen-specific CD8+ cytotoxic and CD4+ helper T cells.
Autologous dendritic cells are loaded ex vivo with patient-specific tumor neoantigen peptides and, upon reinfusion, present these antigens via HLA class I and II to prime and expand neoantigen-specific CD8+ cytotoxic and CD4+ helper T cells, driving tumor-specific immune responses and killing of neoantigen-expressing cancer cells.
YES
INDIRECT
The DC vaccine primes/expands neoantigen-specific T cells; these effector T cells (CD8+ and cytotoxic CD4+) recognize neoantigen–HLA complexes on tumor cells and kill them via perforin/granzyme release and Fas–FasL–mediated apoptosis.
Autologous TCR-T cells engineered via mRNA to transiently express HBV antigen–specific T-cell receptors that recognize HBV peptides presented by HLA-A*02:01 or HLA-A*24:02 on tumor cells, driving TCR/MHC class I–dependent activation and cytotoxicity against HBV-related hepatocellular carcinoma; administered by weekly IV infusion at 5–10×10^6 cells/kg.
Autologous T cells are transiently mRNA-engineered to express HBV-specific T-cell receptors that recognize HBV-derived peptides presented by HLA-A*02:01 or HLA-A*24:02 on tumor cells, triggering TCR/MHC class I–dependent activation and cytotoxic killing of HBV-related hepatocellular carcinoma cells.
YES
DIRECT
Engineered TCR-T cells recognize the HBV peptide–HLA-A*24:02 complex via their TCR, leading to MHC I–dependent activation and killing of target cells through perforin/granzyme (and Fas–FasL) cytotoxic pathways.