Autologous tumor-infiltrating lymphocyte (TIL) adoptive cell therapy composed of ex vivo–expanded patient CD8+/CD4+ TILs reinfused to mediate TCR-dependent recognition and cytotoxic killing of tumor antigen–bearing cells.
Autologous, ex vivo–expanded CD8+/CD4+ tumor-infiltrating T lymphocytes are reinfused to recognize tumor antigen–bearing cells via native TCRs and mediate cytotoxic killing (e.g., perforin/granzyme), leading to antitumor immune responses; product is non–genetically engineered and activity is typically supported by lymphodepletion and IL-2.
YES
DIRECT
Reinfused TILs use native TCRs to recognize the neoantigen peptide–HLA class II complex and directly kill target cells via perforin/granzyme-mediated apoptosis (and Fas–FasL).
Autologous tumor-infiltrating lymphocyte (TIL) adoptive cell therapy composed of ex vivo–expanded patient CD8+/CD4+ TILs reinfused to mediate TCR-dependent recognition and cytotoxic killing of tumor antigen–bearing cells.
Autologous, ex vivo–expanded CD8+/CD4+ tumor-infiltrating T lymphocytes are reinfused to recognize tumor antigen–bearing cells via native TCRs and mediate cytotoxic killing (e.g., perforin/granzyme), leading to antitumor immune responses; product is non–genetically engineered and activity is typically supported by lymphodepletion and IL-2.
YES
DIRECT
TILs recognize the peptide–HLA class II complex via native CD4+ TCRs and directly kill target cells through perforin/granzyme (and Fas–FasL) cytotoxic pathways.
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 MICA via NKG2D, triggering cytotoxic degranulation (perforin/granzyme) and Fas–FasL–mediated apoptosis of target cells.
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 MICB via NKG2D, triggering direct tumor cell killing through 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.
YES
DIRECT
CIK cells recognize ULBP1 via NKG2D in an MHC-unrestricted manner, triggering cytotoxic granule (perforin/granzyme) release and Fas/FasL-mediated apoptosis of target cells.