Autologous or allogeneic T lymphocytes genetically modified to express a chimeric antigen receptor targeting lymphoma antigens for MHC-independent tumor killing.
Autologous or allogeneic T cells are genetically engineered to express a chimeric antigen receptor that binds lymphoma-associated surface antigens (e.g., CD19) independently of MHC. Antigen engagement activates CD3ζ and costimulatory domains (e.g., CD28 or 4-1BB), driving T-cell activation, expansion, and cytotoxic killing of tumor cells via perforin/granzyme release and cytokine production.
CD19 engagement by CAR on engineered T cells activates cytotoxic T-cell killing, primarily via perforin/granzyme-mediated lysis (with additional death receptor/cytokine-mediated apoptosis) of CD19+ cells.
Macrophages engineered to express a chimeric antigen receptor to enhance CAR-directed phagocytosis and remodel the tumor microenvironment.
Macrophages are genetically engineered to express a chimeric antigen receptor (CAR) that confers antigen-specific, MHC-independent recognition of tumor cells. CAR signaling drives targeted phagocytosis of antigen-positive tumor cells, pro-inflammatory activation and cytokine release, enhanced antigen processing/presentation to prime adaptive immunity, and remodeling/repolarization of the tumor microenvironment to overcome immunosuppression.
CAR-expressing macrophages bind the tumor-associated antigen and directly engulf and kill antigen-positive cells via CAR-triggered phagocytosis and phagolysosomal/ROS-mediated cytotoxicity.
T cells engineered to express a tumor-specific T-cell receptor, mediating peptide–HLA–restricted recognition and cytotoxicity.
T cells are genetically engineered to express a tumor-specific T-cell receptor that recognizes peptide antigens presented by specific HLA molecules; upon TCR engagement, the cells activate and mediate MHC/HLA-restricted tumor cell killing via perforin/granzyme release and cytokine-driven cytotoxicity.
Engineered TCR-T cells recognize the tumor peptide–HLA class I complex and directly kill target cells via cytotoxic synapse formation with perforin/granzyme-mediated apoptosis (and Fas–FasL), with cytokine-supported cytotoxicity.
Ex vivo expanded TILs infused to restore antitumor immunity and kill tumor cells via TCR recognition and cytotoxic effector functions.
Autologous TILs are isolated from the tumor, expanded ex vivo, and reinfused as a polyclonal T‑cell product that recognizes tumor antigens via native, HLA‑restricted TCRs and eliminates tumor cells through cytotoxic effector functions (perforin/granzyme) and cytokine release, restoring antitumor immunity without genetic engineering.
Infused TILs recognize neoantigen peptide–HLA class I complexes via native TCRs and directly kill target cells through perforin/granzyme-mediated cytotoxicity (and death-receptor pathways).
Ex vivo expanded TILs infused to restore antitumor immunity and kill tumor cells via TCR recognition and cytotoxic effector functions.
Autologous TILs are isolated from the tumor, expanded ex vivo, and reinfused as a polyclonal T‑cell product that recognizes tumor antigens via native, HLA‑restricted TCRs and eliminates tumor cells through cytotoxic effector functions (perforin/granzyme) and cytokine release, restoring antitumor immunity without genetic engineering.
Infused TILs recognize tumor-associated peptide-HLA class I complexes via their native TCRs and directly kill the target cell through cytolytic granule release (perforin/granzyme) and Fas-FasL–mediated apoptosis.