Autologous T lymphocytes genetically engineered to express a tumor antigen–specific chimeric antigen receptor, used to treat hematologic malignancies and associated with immune effector cell–associated neurotoxicity syndrome (ICANS).
Autologous T cells are genetically engineered to express a chimeric antigen receptor that recognizes a tumor antigen (e.g., CD19). CAR engagement activates CD3ζ and costimulatory domains (such as CD28 or 4‑1BB), leading to T‑cell expansion, cytokine release, and perforin/granzyme‑mediated cytotoxic killing of antigen‑expressing malignant cells; this immune activation can cause toxicities including ICANS.
BCMA-targeted CAR T cells bind BCMA on target cells, triggering CD3ζ/costimulatory signaling and directly killing BCMA+ cells via perforin/granzyme-mediated cytolysis (and Fas/FasL apoptosis).
Allogeneic anti-CD19 CAR T-cell therapy that redirects T cells to CD19 to kill malignant B cells.
Allogeneic, TALEN-edited T cells expressing an anti‑CD19 chimeric antigen receptor bind CD19 on B-lineage tumor cells and trigger T-cell activation and cytolytic killing. TCR alpha knockout reduces graft-versus-host disease risk, and CD52 knockout confers resistance to alemtuzumab used in lymphodepletion to aid engraftment and persistence.
Anti-CD19 CAR T cells bind CD19 on target B cells, form an immunologic synapse, and kill them via T-cell cytotoxic mechanisms (perforin/granzyme release and death-receptor signaling).
Anti-CD52 monoclonal antibody used to deplete CD52-positive host lymphocytes to enhance CAR T-cell engraftment and persistence.
Anti-CD52 monoclonal antibody that binds CD52 on host lymphocytes and mediates immune cell depletion (via complement- and Fc-dependent cytotoxicity) to achieve lymphodepletion and enhance engraftment and persistence of allogeneic CAR T cells.
Anti-CD52 antibody binds CD52 on lymphocytes and induces complement-dependent cytotoxicity and Fc receptor–mediated ADCC, leading to lysis/depletion of CD52+ cells.
An autologous, mRNA-engineered TCR-T cell therapy in which a patient’s T cells are transiently redirected to express HBV antigen–specific T-cell receptors that recognize HBV-derived peptides presented by HLA-A*02:01 or HLA-A*24:02 on tumor cells, inducing TCR/MHC class I–dependent activation and cytotoxic killing of HBV-related hepatocellular carcinoma; administered IV weekly at 5–10×10^6 cells/kg.
Autologous T cells are mRNA-engineered to transiently express HBV-specific T-cell receptors that recognize HBV-derived peptides presented by HLA-A*02:01 or HLA-A*24:02 on tumor cells, triggering TCR/MHC class I–dependent activation and cytotoxic killing of HBV-related hepatocellular carcinoma cells.
Engineered TCR-T cells recognize HBV peptide–HLA-A*02:01 complexes on tumor cells, become activated, and kill them via cytotoxic T-cell effector mechanisms (perforin/granzyme release and Fas–FasL–mediated apoptosis).
An autologous, mRNA-engineered TCR-T cell therapy in which a patient’s T cells are transiently redirected to express HBV antigen–specific T-cell receptors that recognize HBV-derived peptides presented by HLA-A*02:01 or HLA-A*24:02 on tumor cells, inducing TCR/MHC class I–dependent activation and cytotoxic killing of HBV-related hepatocellular carcinoma; administered IV weekly at 5–10×10^6 cells/kg.
Autologous T cells are mRNA-engineered to transiently express HBV-specific T-cell receptors that recognize HBV-derived peptides presented by HLA-A*02:01 or HLA-A*24:02 on tumor cells, triggering TCR/MHC class I–dependent activation and cytotoxic killing of HBV-related hepatocellular carcinoma cells.
mRNA-engineered TCR-T cells recognize the HBV-derived peptide–HLA-A*24:02 complex via their TCR, activating cytotoxic T-cell effector functions that kill target cells through perforin/granzyme release and Fas–FasL–mediated apoptosis.