Engineered natural killer cells expressing an NKG2D-based chimeric antigen receptor; administered via endoscopic ultrasound–guided intratumoral injection plus two intravenous infusions to recognize NKG2D ligands (e.g., MICA, MICB, ULBP family) and induce NK-mediated cytotoxicity.
Engineered NK cells expressing an NKG2D-based chimeric antigen receptor bind NKG2D ligands (e.g., MICA, MICB, ULBP family) on tumor cells, triggering NK activation and cytotoxicity (perforin/granzyme release, cytokine production) to kill cancer cells.
YES
DIRECT
NKG2D CAR-NK cells bind ULBP3 on target cells, triggering NK activation and degranulation to kill the targets via perforin/granzyme–mediated apoptosis.
Engineered natural killer cells expressing an NKG2D-based chimeric antigen receptor; administered via endoscopic ultrasound–guided intratumoral injection plus two intravenous infusions to recognize NKG2D ligands (e.g., MICA, MICB, ULBP family) and induce NK-mediated cytotoxicity.
Engineered NK cells expressing an NKG2D-based chimeric antigen receptor bind NKG2D ligands (e.g., MICA, MICB, ULBP family) on tumor cells, triggering NK activation and cytotoxicity (perforin/granzyme release, cytokine production) to kill cancer cells.
YES
DIRECT
NKG2D CAR-NK cells recognize ULBP4 (an NKG2D ligand) on target cells, triggering NK activation and killing via immune synapse–mediated degranulation (perforin/granzyme) and death-receptor pathways.
Engineered natural killer cells expressing an NKG2D-based chimeric antigen receptor; administered via endoscopic ultrasound–guided intratumoral injection plus two intravenous infusions to recognize NKG2D ligands (e.g., MICA, MICB, ULBP family) and induce NK-mediated cytotoxicity.
Engineered NK cells expressing an NKG2D-based chimeric antigen receptor bind NKG2D ligands (e.g., MICA, MICB, ULBP family) on tumor cells, triggering NK activation and cytotoxicity (perforin/granzyme release, cytokine production) to kill cancer cells.
YES
DIRECT
NKG2D CAR–NK cells bind ULBP5 on target cells, triggering NK activation and release of perforin/granzymes at the immune synapse, causing apoptotic/lytic killing.
Engineered natural killer cells expressing an NKG2D-based chimeric antigen receptor; administered via endoscopic ultrasound–guided intratumoral injection plus two intravenous infusions to recognize NKG2D ligands (e.g., MICA, MICB, ULBP family) and induce NK-mediated cytotoxicity.
Engineered NK cells expressing an NKG2D-based chimeric antigen receptor bind NKG2D ligands (e.g., MICA, MICB, ULBP family) on tumor cells, triggering NK activation and cytotoxicity (perforin/granzyme release, cytokine production) to kill cancer cells.
YES
DIRECT
NKG2D CAR on NK cells binds ULBP6 on target cells, triggering NK activation and degranulation to kill via perforin/granzyme-mediated apoptosis (with possible FasL/TRAIL death-receptor signaling).
Autologous anti-BCMA CAR-T cell therapy (lentiviral-transduced T cells) that binds BCMA on malignant plasma cells/mature B cells and activates T-cell–mediated cytotoxicity.
Autologous T cells are lentiviral-transduced to express a chimeric antigen receptor that targets BCMA on malignant plasma cells/mature B cells; CAR engagement activates T‑cell signaling (CD3ζ with costimulation), leading to targeted cytotoxicity and elimination of BCMA-expressing cells.
YES
DIRECT
Anti-BCMA CAR T cells bind BCMA on target cells; CAR signaling (CD3ζ with costimulation) activates T cells to kill BCMA+ cells via perforin/granzyme release and death-receptor pathways.