Autologous CMV-specific T cells genetically modified to express an anti-CD19 chimeric antigen receptor (CAR); given IV after lymphodepletion to kill CD19+ malignant B cells, with native CMV specificity enabling TCR-mediated boosting by the CMV vaccine.
Autologous CMV-specific T cells engineered to express an anti-CD19 chimeric antigen receptor. The CAR targets CD19 on malignant B cells to activate T-cell cytotoxicity and kill CD19+ cells; the native CMV TCR specificity allows boosting of expansion and persistence upon CMV antigen/vaccine stimulation.
Anti-CD19 CAR T cells recognize CD19 on target cells and induce T-cell cytotoxicity, killing CD19+ cells via perforin/granzyme-mediated lysis (and related effector pathways).
Autologous, gene-engineered T cells expressing a dual chimeric antigen receptor targeting BCMA (TNFRSF17) and GPRC5D on myeloma cells to activate T-cell cytotoxicity and eliminate malignant plasma cells.
Autologous T cells are gene-engineered to express dual chimeric antigen receptors recognizing BCMA (TNFRSF17) and GPRC5D on myeloma cells. Binding triggers CAR signaling (CD3z with costimulatory domains), activating T-cell proliferation, cytokine release, and perforin/granzyme-mediated cytotoxicity to eliminate malignant plasma cells while reducing antigen escape.
CAR-T cells bind BCMA via their CAR, become activated (CD3ζ/costimulatory signaling), form a cytolytic synapse, and kill BCMA+ cells by perforin/granzyme–mediated apoptosis (and potentially Fas–FasL).
Autologous T-cell receptor–engineered T-cell therapy in which patient T cells are lentivirally transduced ex vivo to express an HLA-A*02:01–restricted TCR that recognizes mutant NPM1 (dNPM1) peptides; the cells are expanded and reinfused to mediate antigen-specific cytotoxicity against NPM1-mutant AML.
Autologous T cells are lentivirally transduced ex vivo to express an HLA-A*02:01–restricted T-cell receptor specific for mutant NPM1 (dNPM1) peptides; after expansion and reinfusion, these engineered T cells recognize the HLA-A*02:01/dNPM1 peptide complex on NPM1-mutant AML cells and mediate antigen-specific cytotoxic killing.
Engineered TCR T cells recognize the HLA-A*02:01–presented mutant NPM1 peptide on AML cells and kill them via cytotoxic T-lymphocyte mechanisms (perforin/granzyme release and Fas–FasL–mediated apoptosis).
Autologous, gene-engineered T cells expressing a dual chimeric antigen receptor targeting BCMA (TNFRSF17) and GPRC5D on myeloma cells to activate T-cell cytotoxicity and eliminate malignant plasma cells.
Autologous T cells are gene-engineered to express dual chimeric antigen receptors recognizing BCMA (TNFRSF17) and GPRC5D on myeloma cells. Binding triggers CAR signaling (CD3z with costimulatory domains), activating T-cell proliferation, cytokine release, and perforin/granzyme-mediated cytotoxicity to eliminate malignant plasma cells while reducing antigen escape.
CAR-T cells bind GPRC5D on target cells, triggering T-cell activation and perforin/granzyme-mediated cytolysis (and death-receptor pathways), directly killing GPRC5D+ cells.
Chimeric anti-CD20 monoclonal antibody that depletes CD20-positive B cells from pre-B to mature stages, lowering precursors of ANCA-producing cells.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B to mature B lymphocytes and depletes them via complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity (and apoptosis), reducing precursors of ANCA-producing cells.
Anti-CD20 antibody binds CD20 on B cells and induces complement-dependent cytotoxicity and Fc-mediated ADCC (and apoptosis), leading to depletion of CD20+ cells.