An autologous EBV-targeted chimeric antigen receptor T-cell (CAR-T) therapy for EBV-positive nasopharyngeal carcinoma. Patient T cells are engineered to express a CAR that binds an EBV-specific antigen on tumor cells, triggering CAR signaling, T-cell proliferation, cytokine release, and perforin/granzyme-mediated cytotoxicity. Administered intravenously at 3.0×10^6, 9.0×10^6, or 1.5×10^7 CAR-T cells/kg in this study.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that recognizes an EBV-specific antigen on EBV-positive tumor cells. Antigen engagement triggers CAR signaling, leading to T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of the cancer cells.
CAR-T cells bind the EBV-associated surface antigen and directly lyse antigen-positive tumor cells via T-cell effector functions, primarily perforin/granzyme-mediated cytotoxicity.
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.
Autologous TILs recognize the neoantigen–HLA class I complex via their endogenous TCRs and directly kill target cells through perforin/granzyme-mediated cytolysis and Fas–FasL–induced apoptosis, with proinflammatory cytokines aiding.
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.
Endogenous TCRs on reinfused TILs recognize the tumor-associated peptide–HLA class I complex and directly kill target cells via perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis).
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.
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.
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).