An autologous CLDN18.2-targeted chimeric antigen receptor T-cell (CAR-T) therapy engineered with an NKG2D receptor–based modification to enhance T-cell activation and recognition; mediates cytotoxicity and cytokine release against CLDN18.2-positive tumor cells with added co-stimulation via NKG2D ligands (MICA/B, ULBPs).
Autologous T cells engineered with a chimeric antigen receptor targeting CLDN18.2, augmented with an NKG2D receptor–based module that provides additional co-stimulation via recognition of NKG2D ligands (MICA/B, ULBPs). CAR engagement activates T-cell signaling and, together with NKG2D co-stimulation, drives T-cell activation, cytokine release, and cytolytic killing of CLDN18.2-positive tumor cells.
NO
INDIRECT
IMC008 CAR-T cells execute cytolysis upon CAR engagement of CLDN18.2. The NKG2D-based module binds ULBP2 only to provide co-stimulation, enhancing activation but not conferring killing of ULBP2+ cells by itself.
Lentivirally transduced CAR T cells specific for CD7; IV infusion at escalating doses; designed for MHC-independent cytotoxicity against CD7+ T-cell malignancies.
Autologous/allogeneic T cells are lentivirally engineered to express a chimeric antigen receptor specific for CD7. Upon binding CD7 on malignant T cells, the CAR provides MHC-independent activation (CD3ζ/co-stimulatory signaling), driving T-cell expansion and cytotoxicity via perforin/granzyme release and cytokine-mediated killing of CD7+ tumor cells.
YES
DIRECT
CD7-specific CAR T cells bind CD7 on target cells, become activated via CD3zeta/co-stimulatory signaling, form an immunologic synapse, and directly lyse CD7+ cells through perforin/granzyme release (with additional death-receptor and cytokine-mediated apoptosis).
An autologous CLDN18.2-targeted chimeric antigen receptor T-cell (CAR-T) therapy engineered with an NKG2D receptor–based modification to enhance T-cell activation and recognition; mediates cytotoxicity and cytokine release against CLDN18.2-positive tumor cells with added co-stimulation via NKG2D ligands (MICA/B, ULBPs).
Autologous T cells engineered with a chimeric antigen receptor targeting CLDN18.2, augmented with an NKG2D receptor–based module that provides additional co-stimulation via recognition of NKG2D ligands (MICA/B, ULBPs). CAR engagement activates T-cell signaling and, together with NKG2D co-stimulation, drives T-cell activation, cytokine release, and cytolytic killing of CLDN18.2-positive tumor cells.
NO
INDIRECT
ULBP3 binds the NKG2D costimulatory module to enhance activation of the CLDN18.2 CAR-T cell, but does not by itself trigger killing. Cytolysis (perforin/granzyme) is directed at CLDN18.2-positive cells; ULBP3 provides co-stimulation only, unless co-expressed with CLDN18.2.
An autologous CLDN18.2-targeted chimeric antigen receptor T-cell (CAR-T) therapy engineered with an NKG2D receptor–based modification to enhance T-cell activation and recognition; mediates cytotoxicity and cytokine release against CLDN18.2-positive tumor cells with added co-stimulation via NKG2D ligands (MICA/B, ULBPs).
Autologous T cells engineered with a chimeric antigen receptor targeting CLDN18.2, augmented with an NKG2D receptor–based module that provides additional co-stimulation via recognition of NKG2D ligands (MICA/B, ULBPs). CAR engagement activates T-cell signaling and, together with NKG2D co-stimulation, drives T-cell activation, cytokine release, and cytolytic killing of CLDN18.2-positive tumor cells.
NO
INDIRECT
ULBP4 binds the NKG2D costimulatory module, enhancing activation of CLDN18.2-targeted CAR-T cells but not mediating targeting itself. Killing occurs only when the CAR engages CLDN18.2, with NKG2D–ULBP4 providing co-stimulation to amplify T-cell cytolysis.
An autologous CLDN18.2-targeted chimeric antigen receptor T-cell (CAR-T) therapy engineered with an NKG2D receptor–based modification to enhance T-cell activation and recognition; mediates cytotoxicity and cytokine release against CLDN18.2-positive tumor cells with added co-stimulation via NKG2D ligands (MICA/B, ULBPs).
Autologous T cells engineered with a chimeric antigen receptor targeting CLDN18.2, augmented with an NKG2D receptor–based module that provides additional co-stimulation via recognition of NKG2D ligands (MICA/B, ULBPs). CAR engagement activates T-cell signaling and, together with NKG2D co-stimulation, drives T-cell activation, cytokine release, and cytolytic killing of CLDN18.2-positive tumor cells.
NO
INDIRECT
ULBP5 (an NKG2D ligand) provides co-stimulatory signaling to the CLDN18.2-directed CAR-T cells but is not a primary killing target; cytolysis occurs only when the CAR engages CLDN18.2, with NKG2D–ULBP5 enhancing activation.