Gene-modified T cells bearing a CD19-targeted chimeric antigen receptor and armored to secrete IL-7 and CCL19 to enhance proliferation, survival, and recruitment/trafficking of T cells and dendritic cells for treatment of CD19-positive B-cell lymphomas.
Gene-modified T cells expressing a CD19-specific chimeric antigen receptor to recognize and kill CD19+ B cells via T-cell activation and cytotoxicity; additionally engineered to secrete IL-7 to enhance T-cell survival/proliferation and CCL19 to recruit/traffick T cells and dendritic cells to the tumor, improving infiltration and persistence.
CD19-specific CAR engagement activates the engineered T cells to kill CD19+ cells via perforin/granzyme-mediated cytolysis and death-receptor pathways.
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).
Tumor-specific CTLs recognize patient-specific peptide–HLA class I complexes via their TCR and directly induce apoptosis through perforin/granzyme release (with possible Fas/FasL and NK-like NKG2D contributions).
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 that recognizes MICA on target cells, activating cytotoxic granule release (perforin/granzyme) and causing direct lysis/apoptosis.
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 that recognizes MICB on target cells, activating NK-like cytotoxicity and causing direct lysis via perforin/granzyme release.
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; recognition of ULBP1 on target cells activates cytotoxic granule release (perforin/granzyme) leading to apoptosis/lysis of ULBP1+ cells.