Allogeneic natural killer (NK) cells derived from cord blood and engineered with a chimeric antigen receptor targeting CD19 to mediate NK cytotoxicity (perforin/granzyme) against CD19-positive B-cell malignancies, with low risk of GVHD/CRS.
Allogeneic cord blood–derived natural killer cells genetically engineered with a CD19-directed chimeric antigen receptor. CAR engagement of CD19 on malignant B cells triggers NK activation and perforin/granzyme-mediated cytotoxicity, with low risk of graft-versus-host disease and typically reduced cytokine release compared with CAR-T cells.
YES
DIRECT
CAR engagement of CD19 on target cells activates the NK cell, causing degranulation with perforin and granzymes that induce lysis/apoptosis of CD19+ cells.
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.
YES
DIRECT
CD19-specific CAR engagement activates the engineered T cells to kill CD19+ cells via perforin/granzyme-mediated cytolysis and death-receptor pathways.
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.
NO
INDIRECT
The CAR-T cells target and kill CD19+ B cells via CAR-mediated cytotoxicity. IL-7 secretion engages IL7R (CD127) on T cells to enhance their survival/proliferation; IL7R-expressing cells are not targeted or killed.
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.
NO
INDIRECT
CCR7+ cells are not targeted. The CAR-T cells kill CD19+ cells via CAR-mediated T-cell cytotoxicity (perforin/granzyme). CCL19 secretion binds CCR7 to recruit and support immune cells, not to kill them.
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
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).