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.
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.
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.
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.
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).
Autologous T cells genetically engineered to express a chimeric antigen receptor targeting the EGFRvIII mutant epitope; administered locally to the CNS via an Ommaya reservoir to eliminate EGFRvIII-positive glioblastoma cells through HLA-independent T-cell activation, cytokine release, and cytotoxic killing.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that specifically binds the tumor-specific EGFRvIII epitope on glioblastoma cells, enabling HLA-independent recognition. CAR signaling activates the T cells (via CD3ζ and costimulatory domains), inducing cytokine release, proliferation, and targeted cytotoxic killing of EGFRvIII-positive tumor cells; administered locally to the CNS via an Ommaya reservoir.
CAR-T cells recognize EGFRvIII on tumor cells and, upon CAR activation (CD3ζ/costimulatory), kill targets via perforin/granzyme-mediated cytolysis and apoptosis (HLA-independent).