Autologous TCR-engineered T-cell (TCR-T) therapy in which patient T cells are genetically modified to express an HLA-A*11:01–restricted, HBV-specific T-cell receptor targeting HBV antigen–expressing hepatocellular carcinoma cells; induces TCR signaling, cytokine release, and MHC class I–restricted cytotoxic killing. Administered with step-up induction followed by weekly maintenance infusions.
Autologous T cells are genetically engineered to express an HLA-A*11:01-restricted, HBV-specific T-cell receptor that recognizes HBV peptide–MHC class I complexes on hepatocellular carcinoma cells, activating TCR signaling, cytokine release, and perforin/granzyme-mediated cytotoxic killing.
YES
DIRECT
Engineered TCR-T cells recognize the HBV peptide–HLA-A*11:01 complex on tumor cells and kill them via cytotoxic T-cell mechanisms, primarily perforin/granzyme-mediated lysis (and Fas–FasL apoptosis).
Autologous TCR-engineered T-cell (TCR-T) therapy in which patient T cells are genetically modified to express an HLA-A*11:01–restricted, HBV-specific T-cell receptor targeting HBV antigen–expressing hepatocellular carcinoma cells; induces TCR signaling, cytokine release, and MHC class I–restricted cytotoxic killing. Administered with step-up induction followed by weekly maintenance infusions.
Autologous T cells are genetically engineered to express an HLA-A*11:01-restricted, HBV-specific T-cell receptor that recognizes HBV peptide–MHC class I complexes on hepatocellular carcinoma cells, activating TCR signaling, cytokine release, and perforin/granzyme-mediated cytotoxic killing.
NO
INDIRECT
HLA-A*11:01 expression alone is not sufficient. The engineered TCR-T cells kill only cells presenting the HBV peptide–HLA-A*11:01 complex via TCR engagement, triggering perforin/granzyme-mediated cytolysis.
Autologous, lentiviral-transduced PSMA-directed CAR T-cell therapy with a humanized J591-derived anti-PSMA scFv, CD2 costimulatory domain, and dual armoring via a dominant-negative TGFβ receptor and a PD1.CD28 switch receptor.
Autologous T cells are lentivirally engineered to express a PSMA-specific CAR (humanized J591 scFv) with a CD2 costimulatory domain. The cells are dually armored with a dominant-negative TGF-beta receptor to resist TGF-beta–mediated immunosuppression and a PD1.CD28 switch receptor that converts PD-1 inhibitory signals into CD28 costimulation, enhancing activation, persistence, and cytotoxic killing of PSMA-expressing tumor cells.
YES
DIRECT
PSMA-targeted CAR T cells recognize PSMA on tumor cells and kill them via T-cell effector functions, including perforin/granzyme-mediated cytolysis and death-receptor signaling.
Autologous, lentiviral-transduced PSMA-directed CAR T-cell therapy with a humanized J591-derived anti-PSMA scFv, CD2 costimulatory domain, and dual armoring via a dominant-negative TGFβ receptor and a PD1.CD28 switch receptor.
Autologous T cells are lentivirally engineered to express a PSMA-specific CAR (humanized J591 scFv) with a CD2 costimulatory domain. The cells are dually armored with a dominant-negative TGF-beta receptor to resist TGF-beta–mediated immunosuppression and a PD1.CD28 switch receptor that converts PD-1 inhibitory signals into CD28 costimulation, enhancing activation, persistence, and cytotoxic killing of PSMA-expressing tumor cells.
NO
INDIRECT
Killing is driven by PSMA recognition by the CAR, leading to T cell perforin/granzyme-mediated cytotoxicity; PD-L1 binding via the PD1.CD28 switch receptor provides co-stimulation that enhances killing of PSMA+ cells but does not by itself trigger killing of PD-L1+ cells.
Autologous, lentiviral-transduced PSMA-directed CAR T-cell therapy with a humanized J591-derived anti-PSMA scFv, CD2 costimulatory domain, and dual armoring via a dominant-negative TGFβ receptor and a PD1.CD28 switch receptor.
Autologous T cells are lentivirally engineered to express a PSMA-specific CAR (humanized J591 scFv) with a CD2 costimulatory domain. The cells are dually armored with a dominant-negative TGF-beta receptor to resist TGF-beta–mediated immunosuppression and a PD1.CD28 switch receptor that converts PD-1 inhibitory signals into CD28 costimulation, enhancing activation, persistence, and cytotoxic killing of PSMA-expressing tumor cells.
NO
INDIRECT
CAR T cells kill PSMA-expressing cells via CAR-mediated recognition and perforin/granzyme cytotoxicity. PD-L2 engagement only provides CD28 costimulation through the PD1.CD28 switch receptor and does not make PD-L2+ cells direct cytotoxic targets.