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.
NKG2D on mRNA-enhanced CIK cells binds ULBP4 on target cells, triggering perforin/granzyme-mediated lysis and Fas–FasL–induced apoptosis.
Anti-HER2 monoclonal antibody that inhibits HER2 signaling and mediates ADCC.
Humanized monoclonal antibody that binds HER2 (ERBB2) on tumor cells, blocks HER2 signaling and proliferation, and engages Fc receptors on immune cells to mediate antibody-dependent cellular cytotoxicity (ADCC) against HER2-overexpressing cells.
Trastuzumab binds HER2 on tumor cells and its Fc engages Fcγ receptors on NK cells/macrophages to trigger antibody‑dependent cellular cytotoxicity (ADCC), leading to target cell lysis (with possible complement activation).
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.
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.
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.
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.