Autologous chimeric antigen receptor T-cell product targeting GPRC5D; patient T cells are engineered ex vivo to express an anti-GPRC5D CAR (with CD3ζ signaling and costimulation) and infused intravenously to mediate antigen-specific cytotoxicity against GPRC5D-positive myeloma cells. Dose: 3.0–6.0×10^6 CAR+ T cells/kg.
Autologous T cells are engineered ex vivo to express a chimeric antigen receptor targeting GPRC5D with CD3ζ signaling and costimulatory domains; upon infusion, CAR-T cells bind GPRC5D on myeloma cells, become activated, proliferate, release cytokines, and mediate antigen-specific cytotoxicity (perforin/granzyme) to eliminate GPRC5D-positive malignant plasma cells.
Anti-GPRC5D CAR-T cells bind GPRC5D on target cells and induce cytolysis via immune synapse formation with perforin/granzyme-mediated apoptosis (and Fas/FasL).
Autologous, non-engineered, ex vivo–expanded polyclonal TIL therapy that recognizes tumor antigens via native TCRs and mediates cytotoxicity (perforin/granzyme, cytokines); administered IV at 9×10^10 cells.
Autologous, non-engineered, ex vivo–expanded polyclonal TILs that recognize tumor antigens via native TCR–MHC interactions and kill tumor cells through perforin/granzyme release and cytokine-mediated cytotoxicity after IV infusion.
Adoptively transferred TILs recognize the neoantigen–HLA class I complex via their native TCRs and directly induce tumor-cell death through perforin/granzyme-mediated apoptosis, with contributions from Fas–FasL and cytokine-mediated cytotoxicity.
Autologous, non-engineered, ex vivo–expanded polyclonal TIL therapy that recognizes tumor antigens via native TCRs and mediates cytotoxicity (perforin/granzyme, cytokines); administered IV at 9×10^10 cells.
Autologous, non-engineered, ex vivo–expanded polyclonal TILs that recognize tumor antigens via native TCR–MHC interactions and kill tumor cells through perforin/granzyme release and cytokine-mediated cytotoxicity after IV infusion.
Infused TILs recognize tumor peptide–HLA class I via native TCRs and directly kill targets through perforin/granzyme-mediated apoptosis (with contributions from Fas–FasL and cytokine-mediated cytotoxicity).
Autologous, non-engineered, ex vivo–expanded polyclonal TIL therapy that recognizes tumor antigens via native TCRs and mediates cytotoxicity (perforin/granzyme, cytokines); administered IV at 9×10^10 cells.
Autologous, non-engineered, ex vivo–expanded polyclonal TILs that recognize tumor antigens via native TCR–MHC interactions and kill tumor cells through perforin/granzyme release and cytokine-mediated cytotoxicity after IV infusion.
TILs recognize the neoantigen–HLA class II complex via native TCRs and directly kill the presenting cell through perforin/granzyme release and Fas–FasL–mediated apoptosis, with cytokines (e.g., IFN-γ, TNF) aiding cytotoxicity.
Autologous, non-engineered, ex vivo–expanded polyclonal TIL therapy that recognizes tumor antigens via native TCRs and mediates cytotoxicity (perforin/granzyme, cytokines); administered IV at 9×10^10 cells.
Autologous, non-engineered, ex vivo–expanded polyclonal TILs that recognize tumor antigens via native TCR–MHC interactions and kill tumor cells through perforin/granzyme release and cytokine-mediated cytotoxicity after IV infusion.
Infused TILs recognize the tumor-associated peptide–HLA class II complex via native TCRs and kill the presenting cell through perforin/granzyme release (and Fas–FasL/cytokine-mediated apoptosis).