Gene-modified adoptive T-cell therapy in which donor T cells are lentivirally transduced to express an EBV-specific, HLA-A*02:01/11:01/24:02–restricted T-cell receptor; upon recognizing EBV peptides presented on HLA class I, the engineered T cells kill EBV-infected cells and secrete cytokines.
Donor-derived T cells are lentivirally transduced to express an EBV-specific, HLA-A*02:01/11:01/24:02–restricted T-cell receptor. After infusion, they recognize EBV peptides presented on HLA class I on infected cells, activate via TCR signaling, and mediate cytotoxic killing (perforin/granzyme) with cytokine secretion to eliminate EBV-infected cells and restore antiviral immunity.
Engineered TCR-T cells recognize the EBV peptide–HLA-A*02:01 complex via their TCR and kill target cells through cytotoxic T-cell mechanisms, primarily perforin/granzyme-mediated apoptosis (with possible Fas/FasL contributions).
Gene-modified adoptive T-cell therapy in which donor T cells are lentivirally transduced to express an EBV-specific, HLA-A*02:01/11:01/24:02–restricted T-cell receptor; upon recognizing EBV peptides presented on HLA class I, the engineered T cells kill EBV-infected cells and secrete cytokines.
Donor-derived T cells are lentivirally transduced to express an EBV-specific, HLA-A*02:01/11:01/24:02–restricted T-cell receptor. After infusion, they recognize EBV peptides presented on HLA class I on infected cells, activate via TCR signaling, and mediate cytotoxic killing (perforin/granzyme) with cytokine secretion to eliminate EBV-infected cells and restore antiviral immunity.
EBV-specific TCR-engineered T cells recognize the EBV peptide–HLA-A*11:01 complex via their TCR and directly kill target cells through perforin/granzyme-mediated cytotoxicity.
Gene-modified adoptive T-cell therapy in which donor T cells are lentivirally transduced to express an EBV-specific, HLA-A*02:01/11:01/24:02–restricted T-cell receptor; upon recognizing EBV peptides presented on HLA class I, the engineered T cells kill EBV-infected cells and secrete cytokines.
Donor-derived T cells are lentivirally transduced to express an EBV-specific, HLA-A*02:01/11:01/24:02–restricted T-cell receptor. After infusion, they recognize EBV peptides presented on HLA class I on infected cells, activate via TCR signaling, and mediate cytotoxic killing (perforin/granzyme) with cytokine secretion to eliminate EBV-infected cells and restore antiviral immunity.
Engineered EBV-specific TCRs recognize the EBV peptide–HLA-A*24:02 complex on target cells, triggering immune synapse formation and perforin/granzyme-mediated killing (with possible Fas/FasL apoptosis).
Small-molecule BH3-mimetic BCL-2 inhibitor that restores apoptosis in BCL-2–dependent cells.
Selective BH3-mimetic BCL-2 inhibitor that binds the BH3-binding groove of BCL-2, blocks its anti-apoptotic function, and releases pro-apoptotic proteins to activate BAX/BAK, restoring mitochondrial apoptosis in BCL-2–dependent tumor cells; relatively spares BCL-XL.
Venetoclax directly inhibits BCL-2, releasing pro‑apoptotic proteins to activate BAX/BAK, causing mitochondrial outer membrane permeabilization, caspase activation, and apoptosis in BCL‑2–dependent cells.
Chimeric anti-CD20 IgG1 monoclonal antibody that depletes B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis.
Rituximab is a chimeric anti‑CD20 IgG1 monoclonal antibody that binds CD20 on B cells and induces B‑cell depletion via antibody‑dependent cellular cytotoxicity, complement‑dependent cytotoxicity, and direct apoptosis.
Rituximab binds CD20 on B cells and kills them via Fc-mediated ADCC by NK cells/macrophages, complement-dependent cytotoxicity (C1q activation), and direct apoptotic signaling upon CD20 ligation/crosslinking.