Autologous ex vivo dendritic cell-sensitized cytotoxic T lymphocytes with NK-like cytotoxic features, administered intraperitoneally to kill residual peritoneal tumor cells.
Autologous cytotoxic T lymphocytes expanded ex vivo by dendritic cell sensitization to enrich native TCR tumor specificity; upon intraperitoneal infusion, they kill residual peritoneal tumor cells via antigen-specific TCR recognition and perforin/granzyme release, augmented by NK-like cytotoxic pathways (e.g., NKG2D-mediated killing).
nCTLs express NKG2D; engagement of ULBP2 on target cells activates cytotoxic degranulation (perforin/granzyme) leading to target cell death.
Autologous ex vivo dendritic cell-sensitized cytotoxic T lymphocytes with NK-like cytotoxic features, administered intraperitoneally to kill residual peritoneal tumor cells.
Autologous cytotoxic T lymphocytes expanded ex vivo by dendritic cell sensitization to enrich native TCR tumor specificity; upon intraperitoneal infusion, they kill residual peritoneal tumor cells via antigen-specific TCR recognition and perforin/granzyme release, augmented by NK-like cytotoxic pathways (e.g., NKG2D-mediated killing).
nCTLs use their NKG2D receptor to bind ULBP3 on target cells, triggering degranulation with perforin/granzymes and inducing apoptosis/lysis.
Autologous ex vivo dendritic cell-sensitized cytotoxic T lymphocytes with NK-like cytotoxic features, administered intraperitoneally to kill residual peritoneal tumor cells.
Autologous cytotoxic T lymphocytes expanded ex vivo by dendritic cell sensitization to enrich native TCR tumor specificity; upon intraperitoneal infusion, they kill residual peritoneal tumor cells via antigen-specific TCR recognition and perforin/granzyme release, augmented by NK-like cytotoxic pathways (e.g., NKG2D-mediated killing).
nCTLs use NKG2D to recognize ULBP4 on target cells, triggering cytotoxic degranulation (perforin/granzyme) and killing the target cell.
Autologous ex vivo dendritic cell-sensitized cytotoxic T lymphocytes with NK-like cytotoxic features, administered intraperitoneally to kill residual peritoneal tumor cells.
Autologous cytotoxic T lymphocytes expanded ex vivo by dendritic cell sensitization to enrich native TCR tumor specificity; upon intraperitoneal infusion, they kill residual peritoneal tumor cells via antigen-specific TCR recognition and perforin/granzyme release, augmented by NK-like cytotoxic pathways (e.g., NKG2D-mediated killing).
Infused nCTLs express NKG2D; engagement of ULBP5 (RAET1G) on target cells activates them to release perforin/granzymes, causing apoptosis of the target cell.
Autologous ex vivo dendritic cell-sensitized cytotoxic T lymphocytes with NK-like cytotoxic features, administered intraperitoneally to kill residual peritoneal tumor cells.
Autologous cytotoxic T lymphocytes expanded ex vivo by dendritic cell sensitization to enrich native TCR tumor specificity; upon intraperitoneal infusion, they kill residual peritoneal tumor cells via antigen-specific TCR recognition and perforin/granzyme release, augmented by NK-like cytotoxic pathways (e.g., NKG2D-mediated killing).
nCTLs express NKG2D; engagement of ULBP6 (RAET1L) on target cells activates cytotoxic degranulation (perforin/granzyme), leading to direct lysis.