An autologous tumor-infiltrating lymphocyte (TIL) therapy manufactured from a patient's tumor, containing polyclonal CD8+ and CD4+ T cells that recognize patient-specific tumor antigens via the TCR–MHC pathway and mediate cytotoxic killing.
Autologous, ex vivo–expanded polyclonal CD8+ and CD4+ tumor-infiltrating T cells that recognize patient-specific tumor antigens via TCR–MHC interactions and kill tumor cells through perforin/granzyme-mediated cytotoxicity. Lymphodepleting chemotherapy enhances engraftment, and high-dose IL-2 supports in vivo expansion and persistence.
YES
DIRECT
Adoptively transferred TILs (CD4+ T cells) recognize the tumor-associated peptide presented on MHC class II (HLA-DR/DP/DQ) via their TCR and directly kill target cells through perforin/granzyme release and Fas–FasL–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.
YES
DIRECT
CAR-T cells bind CLDN18.2 on tumor cells, receive activation (with NKG2D co-stimulation), and kill via T-cell cytolysis (perforin/granzyme-mediated apoptosis, plus death-receptor pathways).
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
MICA engages the NKG2D-based co-stimulatory module to enhance activation when the CAR binds CLDN18.2; cytotoxicity is executed against CLDN18.2-positive cells via T-cell perforin/granzyme, not by MICA recognition alone.
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
MICB (an NKG2D ligand) provides co-stimulatory engagement of the NKG2D module, enhancing activation and cytotoxicity of the CAR-T against CLDN18.2-positive cells; MICB expression alone does not trigger direct killing.
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
CAR-T cells kill via CAR recognition of CLDN18.2; ULBP1 (an NKG2D ligand) provides co-stimulation that enhances activation but does not itself trigger direct cytotoxic targeting.