Autologous T cells genetically engineered to express a chimeric antigen receptor targeting CD19; after infusion they eliminate CD19+ B-lineage cells, producing deep and sustained B-cell depletion and a potential immune reset.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that binds CD19 on B-lineage cells. Upon CD19 engagement, the CAR T cells activate and kill target B cells and plasmablasts via perforin/granzyme and death-receptor pathways, causing deep and sustained B-cell depletion, suppression of autoantibody production, and a potential immune reset. Activity is MHC-independent.
YES
DIRECT
CAR T cells bind CD19 on target B-lineage cells and kill them via T-cell cytotoxicity—perforin/granzyme-mediated lysis and death-receptor (e.g., Fas) apoptosis, MHC-independent.
Anti-CD20 monoclonal antibody that depletes CD20+ B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20+ cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells and recruits immune effectors via Fc to mediate ADCC, activates complement for CDC, and can induce apoptosis upon CD20 crosslinking.
Allogeneic, gene-engineered CAR T-cell therapy targeting BCMA (TNFRSF17) and CD19 to deplete B-lineage cells and plasma cells, intended to reduce AQP4-IgG in refractory AQP4-IgG+ NMOSD; dosed at 1.0–4.0 x 10^6 CD3+CAR+ cells/kg.
Allogeneic gene-engineered CAR T cells co-targeting BCMA (TNFRSF17) and CD19; upon antigen engagement they mediate cytotoxic killing of CD19+ B cells and BCMA+ plasmablasts/plasma cells, broadly depleting B-lineage cells and reducing pathogenic AQP4-IgG.
YES
DIRECT
BCMA CAR engagement activates CAR T cells, which kill BCMA+ plasmablasts/plasma cells via perforin/granzyme-mediated cytolysis (and death-receptor pathways).
Allogeneic, gene-engineered CAR T-cell therapy targeting BCMA (TNFRSF17) and CD19 to deplete B-lineage cells and plasma cells, intended to reduce AQP4-IgG in refractory AQP4-IgG+ NMOSD; dosed at 1.0–4.0 x 10^6 CD3+CAR+ cells/kg.
Allogeneic gene-engineered CAR T cells co-targeting BCMA (TNFRSF17) and CD19; upon antigen engagement they mediate cytotoxic killing of CD19+ B cells and BCMA+ plasmablasts/plasma cells, broadly depleting B-lineage cells and reducing pathogenic AQP4-IgG.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 on target B cells and kill them via T-cell cytotoxic mechanisms (perforin/granzyme release and death-receptor pathways).
Autologous T cells genetically modified to express a chimeric antigen receptor targeting CD19 on B cells to mediate cytotoxic killing.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that binds CD19 on B cells, enabling MHC-independent recognition and activation of cytotoxic functions (perforin/granzyme release and cytokine secretion) to eliminate CD19-positive malignant and normal B cells, with in vivo expansion/persistence supporting antitumor activity.
YES
DIRECT
CAR-T cells bind CD19 on target B cells via the CAR, triggering T-cell effector functions (perforin/granzyme-mediated apoptosis, with possible Fas/FasL and cytokine effects) that lyse CD19+ cells.