Autologous mRNA-engineered TCR-T cell therapy in which a patient’s T cells are transiently transfected with mRNA encoding HBV-specific T-cell receptors; infused cells recognize HBV peptides presented by HLA-A*02:01/A*11:01/A*24:02 on infected hepatocytes and mediate MHC class I–restricted cytotoxicity to reduce HBV-infected cells and antigen burden.
Autologous T cells are transiently transfected with mRNA encoding HBV-specific T-cell receptors; after infusion, they recognize HBV peptides presented by HLA-A*02:01/A*11:01/A*24:02 on infected hepatocytes and execute MHC class I–restricted cytotoxicity to reduce HBV-infected cells and antigen burden.
YES
DIRECT
Engineered TCR-T cells recognize HBV peptide–HLA-A*02:01 on target cells and induce MHC I–restricted killing via perforin/granzyme-mediated apoptosis (and Fas–FasL).
Autologous mRNA-engineered TCR-T cell therapy in which a patient’s T cells are transiently transfected with mRNA encoding HBV-specific T-cell receptors; infused cells recognize HBV peptides presented by HLA-A*02:01/A*11:01/A*24:02 on infected hepatocytes and mediate MHC class I–restricted cytotoxicity to reduce HBV-infected cells and antigen burden.
Autologous T cells are transiently transfected with mRNA encoding HBV-specific T-cell receptors; after infusion, they recognize HBV peptides presented by HLA-A*02:01/A*11:01/A*24:02 on infected hepatocytes and execute MHC class I–restricted cytotoxicity to reduce HBV-infected cells and antigen burden.
YES
DIRECT
Autologous TCR-engineered T cells recognize the HBV peptide–HLA-A*11:01 complex on infected cells and kill them via MHC I–restricted cytotoxic T lymphocyte mechanisms (perforin/granzyme-mediated apoptosis, Fas–FasL).
Autologous mRNA-engineered TCR-T cell therapy in which a patient’s T cells are transiently transfected with mRNA encoding HBV-specific T-cell receptors; infused cells recognize HBV peptides presented by HLA-A*02:01/A*11:01/A*24:02 on infected hepatocytes and mediate MHC class I–restricted cytotoxicity to reduce HBV-infected cells and antigen burden.
Autologous T cells are transiently transfected with mRNA encoding HBV-specific T-cell receptors; after infusion, they recognize HBV peptides presented by HLA-A*02:01/A*11:01/A*24:02 on infected hepatocytes and execute MHC class I–restricted cytotoxicity to reduce HBV-infected cells and antigen burden.
YES
DIRECT
Engineered TCR-T cells recognize HBV peptide–HLA-A*24:02 complexes on infected cells and induce MHC I–restricted cytotoxicity via perforin/granzyme release and Fas–FasL–mediated apoptosis.
Autologous tumor-infiltrating lymphocyte (TIL) cell therapy expanded ex vivo and infused IV after lymphodepletion to mediate tumor cell killing via TCR recognition of neoantigens.
Autologous tumor-infiltrating lymphocytes expanded ex vivo are infused after lymphodepletion to recognize patient-specific tumor neoantigens via native TCR–MHC interactions and kill tumor cells through perforin/granzyme-mediated cytotoxicity and cytokine-driven immune activation and persistence.
YES
DIRECT
Autologous TILs recognize the patient-specific neoantigen peptide–HLA class II complex via native TCRs and directly kill target cells through perforin/granzyme release and Fas–FasL–mediated apoptosis.
AZD0901 (CMG901) is an antibody–drug conjugate targeting CLDN18.2; it binds CLDN18.2 on tumor cells, is internalized, and releases a cytotoxic payload to kill CLDN18.2-expressing cells.
Claudin18.2-targeted monoclonal antibody linked via a cleavable linker to MMAE (vedotin). Binds CLDN18.2 on tumor cells, is internalized, and releases MMAE to inhibit tubulin polymerization, causing G2/M arrest and apoptosis in CLDN18.2-expressing cells.
YES
DIRECT
The ADC binds CLDN18.2 on target cells, is internalized, and releases MMAE via a cleavable linker; MMAE disrupts microtubules, causing G2/M arrest and apoptosis of CLDN18.2-expressing cells.