Autologous, gene-edited TCR-engineered T-cell (TCR-T) therapy targeting the KRAS G12V neoantigen presented by HLA-A*11:01; infused T cells recognize KRAS G12V peptide–HLA on tumor cells and mediate cytotoxicity.
Autologous T cells are gene-edited to express a T-cell receptor specific for the KRAS G12V neoantigen presented by HLA-A*11:01. After infusion, these TCR-T cells recognize the KRAS G12V peptide–HLA complex on tumor cells, become activated, and mediate MHC-restricted cytotoxicity (e.g., perforin/granzyme release and cytokine-driven killing).
YES
DIRECT
Engineered TCR-T cells recognize the KRAS G12V peptide presented by HLA-A*11:01 and directly kill target cells via TCR-triggered cytolysis (perforin/granzyme and Fas/FasL-mediated apoptosis).
Autologous, gene-edited TCR-engineered T-cell (TCR-T) therapy targeting the KRAS G12V neoantigen presented by HLA-A*11:01; infused T cells recognize KRAS G12V peptide–HLA on tumor cells and mediate cytotoxicity.
Autologous T cells are gene-edited to express a T-cell receptor specific for the KRAS G12V neoantigen presented by HLA-A*11:01. After infusion, these TCR-T cells recognize the KRAS G12V peptide–HLA complex on tumor cells, become activated, and mediate MHC-restricted cytotoxicity (e.g., perforin/granzyme release and cytokine-driven killing).
NO
DIRECT
Engineered TCR-T cells directly lyse cells only when they present the KRAS G12V peptide in HLA-A*11:01 via perforin/granzyme-mediated killing; HLA-A*11:01 expression alone is not sufficient.
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.
YES
DIRECT
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.
Natural killer cells engineered with a chimeric antigen receptor to direct antigen-specific, MHC-independent cytotoxicity against lymphoma cells.
Natural killer cells are engineered to express a chimeric antigen receptor that enables antigen-specific, MHC-independent recognition of lymphoma cells, triggering NK activation and cytotoxicity (perforin/granzyme release) and cytokine secretion to mediate targeted tumor cell killing.
NO
INDIRECT
CAR‑NK cells directly lyse only cells expressing the CAR-recognized antigen via perforin/granzyme after CAR engagement; with an unknown target, direct killing cannot be assigned.
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.
YES
DIRECT
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.