Patient-derived tumor-infiltrating lymphocytes expanded ex vivo and reinfused after lymphodepletion to mediate tumor-specific cytotoxicity in advanced/metastatic NSCLC.
Autologous tumor-infiltrating T cells are isolated from the patient’s tumor, expanded ex vivo, and reinfused after lymphodepletion. These native T cells recognize tumor-specific antigens via their endogenous TCRs (MHC-restricted) and mediate tumor killing through perforin/granzyme release and cytokine secretion; lymphodepletion (and adjunct PD-1 blockade in the regimen) enhances engraftment, proliferation, and effector function.
YES
DIRECT
TILs recognize the neoantigen peptide–HLA class II complex via their endogenous TCRs and directly lyse target cells through perforin/granzyme release and death-receptor pathways (with cytokine-mediated effects).
Patient-derived tumor-infiltrating lymphocytes expanded ex vivo and reinfused after lymphodepletion to mediate tumor-specific cytotoxicity in advanced/metastatic NSCLC.
Autologous tumor-infiltrating T cells are isolated from the patient’s tumor, expanded ex vivo, and reinfused after lymphodepletion. These native T cells recognize tumor-specific antigens via their endogenous TCRs (MHC-restricted) and mediate tumor killing through perforin/granzyme release and cytokine secretion; lymphodepletion (and adjunct PD-1 blockade in the regimen) enhances engraftment, proliferation, and effector function.
YES
DIRECT
Endogenous TCRs on reinfused TILs recognize the specific peptide–HLA class II complex on target cells, triggering T-cell effector functions that kill the target via perforin/granzyme release and Fas–FasL apoptosis (with supportive cytokines).
Autologous BCMA-directed CAR T-cell therapy administered intravenously; patient T cells are engineered to express a chimeric antigen receptor targeting BCMA on myeloma cells, activating T-cell cytotoxicity and cytokine release to kill BCMA-positive plasma cells.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that binds BCMA on myeloma plasma cells. CAR engagement activates the T cells to proliferate, release cytokines, and mediate perforin/granzyme-dependent cytotoxic killing of BCMA-positive cells.
YES
DIRECT
BCMA-directed CAR T cells bind BCMA on target cells and induce T cell cytotoxicity via perforin/granzyme-mediated lysis (apoptosis).
Subcutaneous bispecific T-cell–redirecting antibody (CD3×GPRC5D) that binds GPRC5D on myeloma cells and CD3 on T cells, recruiting and activating T cells to lyse GPRC5D-positive myeloma cells.
Humanized bispecific antibody that binds CD3 on T cells and GPRC5D on myeloma cells, cross-linking T cells to tumor cells to form an immune synapse and activate cytotoxic T-lymphocyte responses (perforin/granzyme release, cytokine production), leading to lysis of GPRC5D-positive myeloma cells.
YES
DIRECT
Talquetamab crosslinks CD3 on T cells to GPRC5D on target cells, activating T cells to kill GPRC5D+ cells via perforin/granzyme-mediated cytolysis and apoptosis.
Subcutaneous bispecific T-cell–redirecting antibody (CD3×GPRC5D) that binds GPRC5D on myeloma cells and CD3 on T cells, recruiting and activating T cells to lyse GPRC5D-positive myeloma cells.
Humanized bispecific antibody that binds CD3 on T cells and GPRC5D on myeloma cells, cross-linking T cells to tumor cells to form an immune synapse and activate cytotoxic T-lymphocyte responses (perforin/granzyme release, cytokine production), leading to lysis of GPRC5D-positive myeloma cells.
NO
INDIRECT
Talquetamab crosslinks CD3 on T cells to GPRC5D on myeloma cells, activating T cells to release perforin/granzymes and kill GPRC5D+ tumor cells; CD3+ T cells are not the lytic target.