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 ULBP1 on target cells, triggering CD3ζ/costimulatory signaling and T-cell effector functions (perforin/granzyme release, Fas–FasL), leading to MHC-independent lysis/apoptosis of ULBP1-expressing 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 ULBP2 on target cells, triggering CD3ζ/costimulatory signaling and T-cell effector functions that kill the engaged cells via perforin/granzyme-mediated cytolysis (and Fas–FasL), MHC-independently.
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-based CAR-T cells bind ULBP3 on target cells, triggering CD3ζ/costimulatory signaling and T-cell effector functions that kill the target via perforin/granzyme-mediated cytolysis (and apoptosis).
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.
CAR-T cells bind ULBP4 (an NKG2D ligand) on target cells, triggering CD3ζ/costimulatory signaling and T-cell cytotoxicity via perforin/granzyme (and death receptor) pathways, causing MHC-independent lysis/apoptosis.
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-based CAR T cells bind ULBP5 on target cells, activating CD3zeta/costimulatory signaling and inducing perforin/granzyme-mediated lysis (and Fas–FasL apoptosis) of the bound cells.