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.
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.
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.
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.
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.
Autologous anti-CD19 CAR T-cell therapy that targets CD19+ B cells to mediate cytotoxic killing, administered after lymphodepletion.
Autologous T cells engineered with an anti‑CD19 chimeric antigen receptor containing CD3ζ signaling and a 4‑1BB co‑stimulatory domain; after infusion they recognize CD19 on B‑cell malignancies, become activated, expand, and kill CD19+ cells via T‑cell cytotoxic mechanisms.
Anti-CD19 CAR T cells recognize CD19 on target cells and induce killing via T-cell cytotoxic mechanisms, primarily perforin/granzyme-mediated lysis and apoptosis (and Fas–FasL signaling).
Anti-CD20 monoclonal antibody that depletes B cells via ADCC and complement-dependent cytotoxicity.
Rituximab is a chimeric anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes CD20+ cells via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and induction of apoptosis/phagocytosis.
Rituximab binds CD20 on B cells and triggers killing via Fc-mediated ADCC and phagocytosis by immune effector cells, complement-dependent cytotoxicity (CDC), and can induce apoptosis upon crosslinking.