Genetically engineered autologous T cells expressing chimeric antigen receptors targeting CD20 and/or CD30 on lymphoma cells to trigger MHC-independent T-cell activation and cytotoxic killing; given as a single IV infusion after lymphodepleting chemotherapy.
Autologous T cells engineered to express chimeric antigen receptors that bind CD20 and/or CD30 on lymphoma cells, enabling MHC-independent recognition and activation via CD3ζ/costimulatory signaling, leading to T-cell expansion, cytokine release, and cytotoxic killing of CD20+/CD30+ tumor cells after lymphodepleting chemotherapy.
YES
DIRECT
Anti-CD20 CAR-T cells bind CD20 on target cells, activating T-cell cytotoxic programs (perforin/granzyme-mediated lysis and apoptosis, with possible Fas–FasL and cytokine-mediated killing).
Genetically engineered autologous T cells expressing chimeric antigen receptors targeting CD20 and/or CD30 on lymphoma cells to trigger MHC-independent T-cell activation and cytotoxic killing; given as a single IV infusion after lymphodepleting chemotherapy.
Autologous T cells engineered to express chimeric antigen receptors that bind CD20 and/or CD30 on lymphoma cells, enabling MHC-independent recognition and activation via CD3ζ/costimulatory signaling, leading to T-cell expansion, cytokine release, and cytotoxic killing of CD20+/CD30+ tumor cells after lymphodepleting chemotherapy.
YES
DIRECT
CAR-T cells bind CD30 on target cells, become activated, and kill via perforin/granzyme-mediated cytolysis and apoptosis (Fas/FasL), independent of MHC.
Allogeneic NK-92 cell therapy engineered to express a PD-L1–targeting CAR and high-affinity CD16, enabling killing of PD-L1–positive tumor/immunosuppressive cells and ADCC.
Allogeneic NK-92 cells engineered to express a PD-L1–targeting chimeric antigen receptor and high-affinity CD16 (FcγRIIIa), enabling direct killing of PD-L1–positive tumor and immunosuppressive cells and enhancing antibody-dependent cellular cytotoxicity (ADCC).
YES
DIRECT
CAR-engineered NK-92 cells bind PD-L1 on target cells and directly lyse them via NK cytotoxic pathways (perforin/granzyme); high-affinity CD16 also enables ADCC when antibodies are present.
Allogeneic NK-92 cell therapy engineered to express a PD-L1–targeting CAR and high-affinity CD16, enabling killing of PD-L1–positive tumor/immunosuppressive cells and ADCC.
Allogeneic NK-92 cells engineered to express a PD-L1–targeting chimeric antigen receptor and high-affinity CD16 (FcγRIIIa), enabling direct killing of PD-L1–positive tumor and immunosuppressive cells and enhancing antibody-dependent cellular cytotoxicity (ADCC).
NO
INDIRECT
Killing occurs via ADCC: the NK-92 cells’ high‑affinity CD16 binds the IgG1 Fc of therapeutic antibodies opsonizing target cells, triggering NK degranulation and lysis. The IgG1 Fc region itself is not a cellular antigen directly targeted.