Autologous/allogeneic CD3+CD56+ NKT-like effector cells expanded ex vivo; provide MHC-unrestricted cytotoxicity via NKG2D recognition of stress ligands (e.g., MICA/B, ULBPs) and killing through perforin/granzyme and Fas/FasL; used to target B-ALL blasts and support persistence/function of prior CAR-T cells.
Ex vivo–expanded CD3+CD56+ cytokine-induced killer (CIK) cells exert MHC-unrestricted cytotoxicity via NKG2D recognition of stress ligands (e.g., MICA/B, ULBPs) on leukemia cells, mediating killing through perforin/granzyme release and Fas/FasL interactions; they also produce cytokines and can support the persistence and function of previously infused CAR-T cells.
YES
DIRECT
CIK cells recognize ULBP6 via NKG2D, triggering degranulation and killing through perforin/granzyme release and, additionally, Fas–FasL–mediated apoptosis.
Autologous/allogeneic CD3+CD56+ NKT-like effector cells expanded ex vivo; provide MHC-unrestricted cytotoxicity via NKG2D recognition of stress ligands (e.g., MICA/B, ULBPs) and killing through perforin/granzyme and Fas/FasL; used to target B-ALL blasts and support persistence/function of prior CAR-T cells.
Ex vivo–expanded CD3+CD56+ cytokine-induced killer (CIK) cells exert MHC-unrestricted cytotoxicity via NKG2D recognition of stress ligands (e.g., MICA/B, ULBPs) on leukemia cells, mediating killing through perforin/granzyme release and Fas/FasL interactions; they also produce cytokines and can support the persistence and function of previously infused CAR-T cells.
YES
DIRECT
CIK cells express Fas ligand (FasL) that binds Fas (CD95) on target cells, triggering extrinsic apoptosis (death receptor–caspase pathway); they can also kill via perforin/granzyme.
CIK cells transiently enhanced by mRNA modification to boost activity; retain MHC-unrestricted cytotoxicity via NKG2D with perforin/granzyme and Fas/FasL pathways; experimental arm.
mRNA-engineered cytokine-induced killer (CIK) cells that transiently boost activation and cytotoxic function while retaining MHC-unrestricted killing via NKG2D recognition of stress ligands (e.g., MICA/B, ULBPs), mediating tumor cell death through perforin/granzyme release and Fas/FasL pathways.
YES
DIRECT
CIK cells recognize MICA via NKG2D, triggering cytotoxic granule release (perforin/granzyme) and Fas/FasL-mediated apoptosis of target cells.
CIK cells transiently enhanced by mRNA modification to boost activity; retain MHC-unrestricted cytotoxicity via NKG2D with perforin/granzyme and Fas/FasL pathways; experimental arm.
mRNA-engineered cytokine-induced killer (CIK) cells that transiently boost activation and cytotoxic function while retaining MHC-unrestricted killing via NKG2D recognition of stress ligands (e.g., MICA/B, ULBPs), mediating tumor cell death through perforin/granzyme release and Fas/FasL pathways.
YES
DIRECT
CIK cells recognize MICB via NKG2D and directly kill target cells through perforin/granzyme-mediated lysis and Fas/FasL-induced apoptosis (MHC-unrestricted).
CIK cells transiently enhanced by mRNA modification to boost activity; retain MHC-unrestricted cytotoxicity via NKG2D with perforin/granzyme and Fas/FasL pathways; experimental arm.
mRNA-engineered cytokine-induced killer (CIK) cells that transiently boost activation and cytotoxic function while retaining MHC-unrestricted killing via NKG2D recognition of stress ligands (e.g., MICA/B, ULBPs), mediating tumor cell death through perforin/granzyme release and Fas/FasL pathways.
YES
DIRECT
mRNA-CIK cells recognize ULBP1 via NKG2D and directly kill target cells through perforin/granzyme release and Fas–FasL signaling.