Autologous T lymphocytes genetically engineered to express a chimeric antigen receptor targeting tumor-associated antigen(s); administered as a single IV infusion (~1–2×10^6 cells/kg) after fludarabine/cyclophosphamide lymphodepletion to enable expansion and persistence. Mechanism: MHC-independent antigen recognition via CAR with CD3ζ ± costimulatory domains, leading to T-cell activation, cytokine release, and perforin/granzyme-mediated cytotoxic killing.
Autologous T lymphocytes are genetically engineered to express a chimeric antigen receptor that binds tumor-associated antigens independent of MHC, delivering CD3ζ signaling with costimulatory domains to activate T cells. Upon antigen engagement, CAR-T cells expand, release cytokines, and kill target cells via perforin/granzyme and apoptotic pathways. Lymphodepleting chemotherapy (fludarabine/cyclophosphamide) enhances CAR-T expansion and persistence after infusion.
YES
DIRECT
CAR-T cells bind the selected tumor antigen via the CAR, become activated, and kill antigen-expressing cells through perforin/granzyme-mediated cytolysis and death-receptor–mediated apoptosis.
Natural killer cells genetically engineered to express a chimeric antigen receptor to enhance antigen-specific cytotoxicity; given as a single IV infusion (~1–2×10^6 cells/kg) following lymphodepleting chemotherapy. Mechanism: CAR-mediated target recognition combined with innate NK cytotoxic pathways (perforin/granzyme, Fas/TRAIL).
NK cells are genetically engineered to express a chimeric antigen receptor that enables antigen-specific, MHC-independent recognition of tumor cells. CAR engagement activates NK signaling and enhances innate NK cytotoxic mechanisms, leading to target-cell killing via perforin/granzyme release and death-receptor pathways (Fas/TRAIL), along with cytokine secretion to eliminate antigen-expressing tumor cells.
YES
DIRECT
CAR on engineered NK cells binds the tumor antigen, triggering NK activation and killing antigen-positive cells via perforin/granzyme release and death-receptor pathways (FasL/TRAIL).
Natural killer cells genetically engineered to express a chimeric antigen receptor to enhance antigen-specific cytotoxicity; given as a single IV infusion (~1–2×10^6 cells/kg) following lymphodepleting chemotherapy. Mechanism: CAR-mediated target recognition combined with innate NK cytotoxic pathways (perforin/granzyme, Fas/TRAIL).
NK cells are genetically engineered to express a chimeric antigen receptor that enables antigen-specific, MHC-independent recognition of tumor cells. CAR engagement activates NK signaling and enhances innate NK cytotoxic mechanisms, leading to target-cell killing via perforin/granzyme release and death-receptor pathways (Fas/TRAIL), along with cytokine secretion to eliminate antigen-expressing tumor cells.
YES
INDIRECT
CAR engagement activates NK cells, which express FasL that binds FAS (CD95) on target cells to trigger death‑receptor (caspase-mediated) apoptosis; perforin/granzyme may also contribute.
Natural killer cells genetically engineered to express a chimeric antigen receptor to enhance antigen-specific cytotoxicity; given as a single IV infusion (~1–2×10^6 cells/kg) following lymphodepleting chemotherapy. Mechanism: CAR-mediated target recognition combined with innate NK cytotoxic pathways (perforin/granzyme, Fas/TRAIL).
NK cells are genetically engineered to express a chimeric antigen receptor that enables antigen-specific, MHC-independent recognition of tumor cells. CAR engagement activates NK signaling and enhances innate NK cytotoxic mechanisms, leading to target-cell killing via perforin/granzyme release and death-receptor pathways (Fas/TRAIL), along with cytokine secretion to eliminate antigen-expressing tumor cells.
YES
INDIRECT
Upon CAR engagement with their specific antigen (not DR4), CAR‑NK cells kill via death‑receptor pathways; NK‑expressed TRAIL binds TRAIL‑R1 (DR4) on target cells, triggering extrinsic apoptosis.
Natural killer cells genetically engineered to express a chimeric antigen receptor to enhance antigen-specific cytotoxicity; given as a single IV infusion (~1–2×10^6 cells/kg) following lymphodepleting chemotherapy. Mechanism: CAR-mediated target recognition combined with innate NK cytotoxic pathways (perforin/granzyme, Fas/TRAIL).
NK cells are genetically engineered to express a chimeric antigen receptor that enables antigen-specific, MHC-independent recognition of tumor cells. CAR engagement activates NK signaling and enhances innate NK cytotoxic mechanisms, leading to target-cell killing via perforin/granzyme release and death-receptor pathways (Fas/TRAIL), along with cytokine secretion to eliminate antigen-expressing tumor cells.
YES
DIRECT
Activated CAR-NK cells express TRAIL that binds DR5 (TRAIL-R2) on target cells, triggering death-receptor (extrinsic) apoptosis via caspase-8; NK cells may also kill via perforin/granzyme.