Autologous T cells genetically engineered to express a single CAR with tandem scFvs targeting CD19 and CD20, incorporating a 4-1BB co-stimulatory and CD3ζ signaling domain to activate, expand, and mediate cytotoxic killing of malignant B cells; dual targeting aims to reduce antigen-loss escape.
Autologous T cells are genetically engineered to express a single CAR with tandem scFvs targeting CD19 and CD20, incorporating a 4-1BB co-stimulatory and CD3zeta signaling domain. Binding to CD19 or CD20 activates and expands the CAR T cells, driving targeted cytotoxic killing of malignant B cells and reducing antigen-loss escape.
YES
DIRECT
CAR T cells recognize CD19 via the CAR and, upon CD3ζ/4-1BB activation, kill target cells through perforin/granzyme-mediated cytolysis and apoptotic pathways.
Personalized cellular immunotherapy using patient-derived tumor-resident T cells (primarily CD8+ and CD4+) expanded ex vivo and reinfused as a single IV infusion (e.g., 2.0×10^7 cells/kg) to recognize tumor/neoantigens via TCR–MHC interactions and mediate cytotoxicity through perforin/granzyme and cytokine release.
Autologous tumor-resident T cells (CD8+/CD4+) expanded ex vivo and reinfused; they recognize patient-specific tumor/neoantigens via native TCR–MHC I/II interactions and mediate cytotoxicity through perforin/granzyme release and cytokine secretion (e.g., IFN-γ, TNF-α), enhancing antitumor immunity within the tumor microenvironment.
YES
DIRECT
Autologous TILs use native TCRs to recognize AFP-derived peptides presented on MHC (primarily class I) on tumor cells, then kill them via cytotoxic T-cell effector mechanisms (perforin/granzyme and Fas–FasL), with supportive cytokines.
Autologous T cells genetically engineered to express a single CAR with tandem scFvs targeting CD19 and CD20, incorporating a 4-1BB co-stimulatory and CD3ζ signaling domain to activate, expand, and mediate cytotoxic killing of malignant B cells; dual targeting aims to reduce antigen-loss escape.
Autologous T cells are genetically engineered to express a single CAR with tandem scFvs targeting CD19 and CD20, incorporating a 4-1BB co-stimulatory and CD3zeta signaling domain. Binding to CD19 or CD20 activates and expands the CAR T cells, driving targeted cytotoxic killing of malignant B cells and reducing antigen-loss escape.
YES
DIRECT
CAR T cells bind CD20 via the tandem CAR, become activated through CD3ζ/4-1BB signaling, and kill CD20+ cells via perforin/granzyme-mediated cytolysis (and death-receptor pathways).
A personalized mRNA cancer vaccine encoding patient-specific tumor neoantigens; the mRNA is taken up by host antigen-presenting cells, translated, and presented via HLA to prime and expand neoantigen-specific CD8+ and CD4+ T cells.
Personalized mRNA encoding patient-specific tumor neoantigens is taken up by host antigen-presenting cells, translated into neoantigen peptides, processed and presented on HLA class I and II, thereby priming and expanding neoantigen-specific CD8+ cytotoxic and CD4+ helper T cells to drive antitumor immunity.
YES
INDIRECT
The vaccine primes and expands neoantigen-specific CD8+ T cells via APC presentation; these T cells recognize HLA-I–presented neoepitopes on tumor cells and kill them via perforin/granzyme and Fas–FasL pathways.
A personalized mRNA cancer vaccine encoding patient-specific tumor neoantigens; the mRNA is taken up by host antigen-presenting cells, translated, and presented via HLA to prime and expand neoantigen-specific CD8+ and CD4+ T cells.
Personalized mRNA encoding patient-specific tumor neoantigens is taken up by host antigen-presenting cells, translated into neoantigen peptides, processed and presented on HLA class I and II, thereby priming and expanding neoantigen-specific CD8+ cytotoxic and CD4+ helper T cells to drive antitumor immunity.
YES
INDIRECT
The mRNA vaccine primes neoantigen-specific T cells. Vaccine-induced CD4 (and CD8) T cells recognize tumor cells presenting the neoepitopes (HLA-II for CD4; HLA-I for CD8) and kill them via TCR-dependent cytotoxicity (perforin/granzyme and/or Fas–FasL), not by the drug directly.