Autologous tumor-infiltrating lymphocyte (TIL) product; patient-derived TILs are isolated from the tumor, expanded ex vivo, and reinfused to recognize tumor neoantigens/tumor-associated antigens via the T-cell receptor, mediating CD8+ cytotoxicity (perforin/granzyme, IFN-γ) with CD4+ support.
Autologous tumor-infiltrating lymphocytes isolated from the patient’s tumor are expanded ex vivo and reinfused. These T cells recognize tumor neoantigens/tumor-associated antigens via their native T-cell receptors (MHC-restricted) and mediate anti-tumor activity through CD8+ cytotoxicity (perforin/granzyme, IFN-γ) with CD4+ T-cell support, enhancing local immune attack and remodeling the tumor microenvironment.
YES
DIRECT
Autologous TILs recognize tumor-associated peptides presented on MHC I via their native TCRs and directly induce apoptosis of target cells through CD8+ cytotoxicity (perforin/granzyme and Fas–FasL), with IFN-γ support.
Autologous tumor-infiltrating lymphocyte (TIL) product; patient-derived TILs are isolated from the tumor, expanded ex vivo, and reinfused to recognize tumor neoantigens/tumor-associated antigens via the T-cell receptor, mediating CD8+ cytotoxicity (perforin/granzyme, IFN-γ) with CD4+ support.
Autologous tumor-infiltrating lymphocytes isolated from the patient’s tumor are expanded ex vivo and reinfused. These T cells recognize tumor neoantigens/tumor-associated antigens via their native T-cell receptors (MHC-restricted) and mediate anti-tumor activity through CD8+ cytotoxicity (perforin/granzyme, IFN-γ) with CD4+ T-cell support, enhancing local immune attack and remodeling the tumor microenvironment.
YES
DIRECT
Native TCRs on infused TILs (CD4+ T cells) recognize patient-specific neoantigen peptides presented on MHC II (HLA-DR/DQ/DP) and directly kill target cells via perforin/granzyme and Fas–FasL pathways, with IFN-γ supporting cytotoxic activity.
Autologous tumor-infiltrating lymphocyte (TIL) product; patient-derived TILs are isolated from the tumor, expanded ex vivo, and reinfused to recognize tumor neoantigens/tumor-associated antigens via the T-cell receptor, mediating CD8+ cytotoxicity (perforin/granzyme, IFN-γ) with CD4+ support.
Autologous tumor-infiltrating lymphocytes isolated from the patient’s tumor are expanded ex vivo and reinfused. These T cells recognize tumor neoantigens/tumor-associated antigens via their native T-cell receptors (MHC-restricted) and mediate anti-tumor activity through CD8+ cytotoxicity (perforin/granzyme, IFN-γ) with CD4+ T-cell support, enhancing local immune attack and remodeling the tumor microenvironment.
YES
DIRECT
TILs recognize tumor-associated peptides on HLA class II via native TCRs; CD4+ T cells directly lyse presenting cells through perforin/granzyme and Fas-FasL, with IFN-γ enhancing cytotoxicity.
Autologous dual-target CAR T-cell therapy in which the patient’s T cells are engineered to express chimeric antigen receptors recognizing BCMA and GPRC5D; administered by IV infusion to activate T-cell cytotoxicity against multiple myeloma cells.
Autologous T cells are engineered to express dual chimeric antigen receptors targeting BCMA and GPRC5D on myeloma cells; antigen binding triggers CAR signaling (CD3 zeta with co-stimulation), activating T-cell cytokine release and perforin/granzyme-mediated cytotoxic killing, with dual targeting intended to reduce antigen escape.
YES
DIRECT
CAR T cells bind BCMA via the CAR, triggering CD3ζ/co-stimulatory signaling and release of perforin and granzymes to lyse BCMA-expressing cells.
Autologous dual-target CAR T-cell therapy in which the patient’s T cells are engineered to express chimeric antigen receptors recognizing BCMA and GPRC5D; administered by IV infusion to activate T-cell cytotoxicity against multiple myeloma cells.
Autologous T cells are engineered to express dual chimeric antigen receptors targeting BCMA and GPRC5D on myeloma cells; antigen binding triggers CAR signaling (CD3 zeta with co-stimulation), activating T-cell cytokine release and perforin/granzyme-mediated cytotoxic killing, with dual targeting intended to reduce antigen escape.
YES
DIRECT
CAR T cells recognize GPRC5D on tumor cells via the CAR, triggering CD3z/co-stimulatory signaling that activates T-cell degranulation and perforin/granzyme-mediated apoptosis (and Fas/FasL/cytokine-mediated killing).