Universal chimeric natural killer receptor–modified T cells engineered to dual-target NKG2D and NKp44 (NCR2) ligands on tumors, triggering T-cell cytotoxicity and cytokine release.
T cells engineered with NK receptor–based chimeric receptors that dual-target ligands for NKG2D and NKp44 (NCR2) on tumor cells; ligand engagement triggers T‑cell activation signaling to drive cytotoxic killing and cytokine release, addressing antigen heterogeneity in solid tumors.
YES
DIRECT
NK receptor–based CAR T cells recognize the NKG2D ligand ULBP4, activating T-cell signaling and cytolytic degranulation (perforin/granzymes) to kill the target cells.
Autologous T lymphocytes engineered with a CD19-directed chimeric antigen receptor to recognize and kill CD19-positive B cells in hematologic malignancies, leading to B-cell aplasia and hypogammaglobulinemia.
Autologous T lymphocytes engineered to express a CD19‑directed chimeric antigen receptor (with CD3ζ and costimulatory signaling domains) bind CD19 on malignant and normal B cells, triggering T‑cell activation, proliferation, cytokine release, and cytotoxic killing via perforin/granzyme pathways, resulting in depletion of CD19+ cells and consequent B‑cell aplasia and hypogammaglobulinemia.
YES
DIRECT
CD19-targeted CAR T cells bind CD19 on B cells and induce T‑cell cytotoxicity via perforin/granzyme (and Fas–FasL) pathways, causing apoptosis of CD19+ cells.
An anti-HER2 antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and releases the cytotoxic payload MMAE to inhibit microtubule polymerization, causing mitotic arrest and apoptosis; may also mediate ADCC.
Anti-HER2 antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and releases the cytotoxic payload MMAE to inhibit microtubule polymerization, leading to mitotic arrest and apoptosis; may also mediate Fc-dependent ADCC.
NO
INDIRECT
The ADC binds HER2 (not beta-tubulin), is internalized, and releases MMAE, which binds the beta‑tubulin vinca site to block microtubule polymerization, causing mitotic arrest and apoptosis. Beta‑tubulin is the payload’s intracellular target, not the directly targeted antigen.
Cord blood–derived natural killer (NK) cells genetically engineered to express a CD19-directed chimeric antigen receptor for antigen-specific recognition and cytotoxic killing of CD19-positive B cells in B-cell malignancies.
Cord blood–derived NK cells are engineered to express a CD19-specific chimeric antigen receptor, enabling antigen-dependent recognition and cytotoxic killing of CD19-positive B cells in B-cell malignancies. In this construct, IL-15 supports NK activation, proliferation, and persistence, while IL-10 modulates inflammatory responses to enhance antitumor activity and potentially reduce toxicity.
NO
INDIRECT
Anti-CD19 CAR-NK cells recognize CD19 and kill CD19-positive B cells via CAR-triggered NK cytotoxicity (perforin/granzyme). The common gamma chain is not a recognized target; it functions in IL-15 signaling to support NK activation and persistence, so cells expressing it are not directly killed.
Universal chimeric natural killer receptor–modified T cells engineered to dual-target NKG2D and NKp44 (NCR2) ligands on tumors, triggering T-cell cytotoxicity and cytokine release.
T cells engineered with NK receptor–based chimeric receptors that dual-target ligands for NKG2D and NKp44 (NCR2) on tumor cells; ligand engagement triggers T‑cell activation signaling to drive cytotoxic killing and cytokine release, addressing antigen heterogeneity in solid tumors.
YES
DIRECT
ULBP5 is an NKG2D ligand; CNK-UT T cells use NKG2D-based CARs to bind ULBP5, activating T-cell cytotoxic pathways (perforin/granzyme) and killing ULBP5+ cells.