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.
YES
DIRECT
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.
YES
DIRECT
NKG2D CAR-T cells bind MICB on target cells, triggering CD3ζ/costimulatory signaling and killing via perforin/granzyme-mediated cytotoxicity (and death-receptor pathways).
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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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).