Autologous T lymphocytes genetically engineered to express a CD7-directed chimeric antigen receptor; administered intravenously with dose escalation to activate, proliferate, and kill CD7-positive leukemic cells via perforin/granzyme cytotoxicity, causing depletion of CD7+ malignant cells and on-target T/NK-cell aplasia.
Autologous T cells engineered to express a CD7-directed chimeric antigen receptor; CAR engagement with CD7 triggers CD3ζ and costimulatory signaling, activating and expanding the T cells to mediate MHC-independent cytotoxicity (perforin/granzyme and cytokine release) against CD7-positive leukemic cells, resulting in depletion of CD7+ malignant cells and on-target T/NK-cell aplasia.
CD7 CAR-T cells bind CD7 on target cells, triggering CAR (CD3zeta and costimulatory) signaling and directly lysing CD7-positive cells via perforin/granzyme-mediated cytotoxicity (MHC-independent).
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.
CIK cells express NKG2D; binding to ULBP4 on target cells activates MHC-unrestricted killing via perforin/granzyme release and 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.
CIK cells express NKG2D, which binds ULBP5 on target cells and triggers MHC-unrestricted cytotoxicity via perforin/granzyme release and Fas/FasL interactions.
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.
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.
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.