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.
NKG2D CAR-NK cells bind ULBP2 on target cells, triggering NK activation and degranulation (perforin/granzyme–mediated apoptosis), with possible contribution from death receptor pathways (FasL/TRAIL).
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.
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.
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.
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.
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).