Allogeneic gamma-delta T cells engineered by mRNA electroporation to transiently express an NKG2D-based CAR that binds NKG2D ligands (MICA/MICB, ULBP1-6) on stressed tumor and tumor microenvironment cells; engagement activates CAR and native gamma-delta TCR/DNAM-1 signaling to drive pro-inflammatory cytokine release and MHC-independent cytotoxic killing.
YES
DIRECT
NKG2D-CAR on engineered γδ T cells binds ULBP3 on target cells, activating CAR/γδ T-cell signaling to mediate MHC-independent killing via perforin/granzyme and pro-inflammatory cytokines.
Allogeneic gamma-delta T cells engineered by mRNA electroporation to transiently express an NKG2D-based CAR that binds NKG2D ligands (MICA/MICB, ULBP1-6) on stressed tumor and tumor microenvironment cells; engagement activates CAR and native gamma-delta TCR/DNAM-1 signaling to drive pro-inflammatory cytokine release and MHC-independent cytotoxic killing.
YES
DIRECT
Engineered gamma-delta T cells expressing an NKG2D-based CAR bind ULBP4 (an NKG2D ligand) on target cells, activating CAR and native signaling to deliver perforin/granzyme-mediated, MHC-independent cytotoxic killing.
An anti-HER2 antibody–drug conjugate that binds HER2 (ERBB2), is internalized, and releases the microtubule inhibitor MMAE to induce mitotic arrest and apoptosis.
Anti-HER2 monoclonal antibody linked to MMAE. Binds HER2 (ERBB2) on tumor cells, is internalized, and releases the microtubule inhibitor MMAE intracellularly, causing mitotic arrest and apoptosis.
NO
INDIRECT
The ADC targets HER2, is internalized, and releases MMAE that binds beta-tubulin to disrupt microtubules, causing mitotic arrest and apoptosis; tubulin expression alone is not directly targeted.
Allogeneic gamma-delta T cells engineered by mRNA electroporation to transiently express an NKG2D-based CAR that binds NKG2D ligands (MICA/MICB, ULBP1-6) on stressed tumor and tumor microenvironment cells; engagement activates CAR and native gamma-delta TCR/DNAM-1 signaling to drive pro-inflammatory cytokine release and MHC-independent cytotoxic killing.
YES
DIRECT
NKG2D-CAR–engineered gamma-delta T cells bind ULBP5 on target cells, triggering CAR (and native γδ/DNAM-1) signaling, degranulation, and perforin/granzyme-mediated MHC-independent cytolysis with pro-inflammatory cytokine release.
Allogeneic gamma-delta T cells engineered by mRNA electroporation to transiently express an NKG2D-based CAR that binds NKG2D ligands (MICA/MICB, ULBP1-6) on stressed tumor and tumor microenvironment cells; engagement activates CAR and native gamma-delta TCR/DNAM-1 signaling to drive pro-inflammatory cytokine release and MHC-independent cytotoxic killing.
YES
DIRECT
Engineered γδ T cells expressing an NKG2D-based CAR bind ULBP6 on target cells, triggering CAR and native γδ TCR/DNAM-1 signaling that induces degranulation (perforin/granzyme) and MHC-independent cytolytic killing.