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).
YES
DIRECT
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).
YES
DIRECT
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).
YES
DIRECT
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).
YES
DIRECT
nCTLs express NKG2D; engagement of ULBP6 (RAET1L) on target cells activates cytotoxic degranulation (perforin/granzyme), leading to direct lysis.
Autologous, gene-modified bispecific CD19/CD20-directed CAR T-cell therapy designed to deplete B-lineage cells to suppress B-cell–driven autoimmunity in refractory SLE and lupus nephritis.
Autologous T cells are gene-modified to express a bispecific CAR targeting CD19 and CD20 on B-lineage cells; engagement activates the CAR T cells to kill and deplete B cells and plasmablasts, reducing autoantibody production and B cell–driven autoimmunity in SLE and lupus nephritis.
YES
DIRECT
CAR T cells bind CD19 on B-lineage cells via the bispecific CD19/CD20 CAR, triggering T-cell activation and immune-synapse formation, leading to perforin/granzyme-mediated cytolysis and apoptosis of CD19+ cells.