Autologous CAR-T cells engineered to target the immune checkpoint ligand B7-H3 (CD276), promoting T-cell activation and cytotoxicity against B7-H3–positive solid tumors upon reinfusion.
Autologous T cells are engineered to express a chimeric antigen receptor that binds B7-H3 (CD276) on tumor cells. Antigen engagement triggers CD3 zeta and costimulatory signaling in an MHC-independent manner, driving T-cell activation, proliferation, cytokine release, and cytotoxic killing of B7-H3-positive solid tumor cells.
CAR-T cells recognize B7-H3 on target cells and, upon CAR activation, kill them via perforin/granzyme-mediated cytolysis and apoptosis (Fas–FasL/cytokine effects).
Autologous CAR-T cells engineered to recognize CD19 on B-lineage malignancies, inducing T-cell activation and tumor cell lysis in an MHC-independent manner after reinfusion.
Autologous T cells are engineered to express a chimeric antigen receptor that binds CD19 on B-lineage tumor cells in an MHC-independent manner, triggering T-cell activation (CD3ζ with costimulatory signaling), cytokine release, proliferation, and cytotoxic killing of CD19-positive cells.
CAR-T cells recognize CD19 and, upon engagement, directly kill target cells via perforin/granzyme-mediated cytolysis and death-receptor pathways (e.g., Fas–FasL).
Autologous CAR-T cells engineered to target BCMA (TNFRSF17) on plasma cells, enabling MHC-independent recognition and cytotoxic killing of BCMA-expressing hematologic malignancies.
Autologous T cells are engineered with a chimeric antigen receptor that binds BCMA (TNFRSF17) on plasma cells, enabling MHC-independent recognition. Antigen engagement triggers CAR signaling (CD3ζ with costimulatory domains such as CD28 or 4‑1BB), leading to T‑cell activation, proliferation, cytokine release, and perforin/granzyme‑mediated cytotoxic killing of BCMA‑expressing malignant plasma cells (e.g., multiple myeloma).
BCMA-directed CAR-T cells bind BCMA on target cells, triggering T-cell activation and perforin/granzyme-mediated cytotoxic apoptosis (± Fas–FasL).
Autologous CAR-T cells incorporating an NKG2D-based receptor to bind stress-induced ligands (e.g., MICA, MICB, ULBPs) on tumor cells, triggering T-cell activation and cytotoxicity across diverse tumors.
Autologous T cells engineered to express an NKG2D-based chimeric antigen receptor that binds stress-induced ligands (e.g., MICA, MICB, ULBPs) on tumor cells, initiating CD3ζ/costimulatory signaling to activate T cells, drive cytokine release and proliferation, and mediate MHC-independent cytotoxic tumor killing.
NKG2D-CAR T cells bind MICA on target cells, triggering CD3ζ/costimulatory signaling and releasing perforin/granzymes to induce cytolysis/apoptosis of the bound cells.
Autologous CAR-T cells incorporating an NKG2D-based receptor to bind stress-induced ligands (e.g., MICA, MICB, ULBPs) on tumor cells, triggering T-cell activation and cytotoxicity across diverse tumors.
Autologous T cells engineered to express an NKG2D-based chimeric antigen receptor that binds stress-induced ligands (e.g., MICA, MICB, ULBPs) on tumor cells, initiating CD3ζ/costimulatory signaling to activate T cells, drive cytokine release and proliferation, and mediate MHC-independent cytotoxic tumor killing.
NKG2D CAR-T cells bind MICB on target cells, triggering CD3ζ/costimulatory signaling and killing via perforin/granzyme-mediated cytotoxicity (and death-receptor pathways).