CIK cells transiently enhanced by mRNA modification to boost activity; retain MHC-unrestricted cytotoxicity via NKG2D with perforin/granzyme and Fas/FasL pathways; experimental arm.
mRNA-engineered cytokine-induced killer (CIK) cells that transiently boost activation and cytotoxic function while retaining MHC-unrestricted killing via NKG2D recognition of stress ligands (e.g., MICA/B, ULBPs), mediating tumor cell death through perforin/granzyme release and Fas/FasL pathways.
YES
DIRECT
mRNA-enhanced CIK cells engage ULBP5 via NKG2D, triggering cytotoxic granule (perforin/granzyme) release and Fas–FasL–mediated apoptosis of target cells.
CIK cells transiently enhanced by mRNA modification to boost activity; retain MHC-unrestricted cytotoxicity via NKG2D with perforin/granzyme and Fas/FasL pathways; experimental arm.
mRNA-engineered cytokine-induced killer (CIK) cells that transiently boost activation and cytotoxic function while retaining MHC-unrestricted killing via NKG2D recognition of stress ligands (e.g., MICA/B, ULBPs), mediating tumor cell death through perforin/granzyme release and Fas/FasL pathways.
YES
DIRECT
NKG2D on mRNA-modified CIK cells binds ULBP6 on target cells, triggering cytotoxic degranulation (perforin/granzyme) and Fas–FasL–mediated apoptosis.
CIK cells transiently enhanced by mRNA modification to boost activity; retain MHC-unrestricted cytotoxicity via NKG2D with perforin/granzyme and Fas/FasL pathways; experimental arm.
mRNA-engineered cytokine-induced killer (CIK) cells that transiently boost activation and cytotoxic function while retaining MHC-unrestricted killing via NKG2D recognition of stress ligands (e.g., MICA/B, ULBPs), mediating tumor cell death through perforin/granzyme release and Fas/FasL pathways.
YES
DIRECT
FasL on mRNA-CIK cells binds Fas (CD95) on target cells, triggering extrinsic apoptosis via Fas–FasL signaling (caspase-8), in addition to perforin/granzyme cytotoxicity.
Autologous T cells genetically engineered to express a HER2 (ERBB2)-specific chimeric antigen receptor, enabling recognition and killing of HER2-expressing tumor cells via T-cell activation and cytokine release.
Autologous T cells engineered to express a HER2-specific chimeric antigen receptor bind HER2 on tumor cells, triggering T‑cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of HER2-expressing cells.
YES
DIRECT
HER2-specific CAR-T cells bind HER2 on target cells, activate, form an immune synapse, and kill via perforin/granzyme-mediated cytolysis (and Fas–FasL), with accompanying cytokine release.
Human IgG1κ monoclonal antibody targeting CD38; mediates Fc-dependent ADCC and ADCP, complement-dependent cytotoxicity (CDC), and apoptosis, and depletes CD38+ immunosuppressive cells to remodel the tumor microenvironment.
Human IgG1κ monoclonal antibody targeting CD38 that induces tumor-cell killing via Fc-dependent ADCC and ADCP, complement-dependent cytotoxicity, and apoptosis, while depleting CD38+ immunosuppressive cells to remodel the tumor microenvironment.
YES
DIRECT
Anti-CD38 IgG1 binds CD38 on target cells and induces Fc-dependent ADCC by NK cells, ADCP by macrophages, complement-dependent cytotoxicity (CDC), and can trigger apoptosis upon crosslinking.