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.
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.
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.
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.
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.
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.
ULBP6 is an NKG2D ligand; binding to the NKG2D-based chimeric receptor on the engineered T cells activates them to kill target cells via perforin/granzyme-mediated cytolysis and apoptosis, with cytokine release.
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.
Engineered T cells bearing NK receptor–based chimeric receptors bind NKp44 ligands on tumor cells, triggering T-cell activation and perforin/granzyme-mediated cytolysis (with cytokine release).