Autologous, genetically engineered anti-CD19/CD20 chimeric antigen receptor (CAR) T-cell therapy; single IV infusion designed to deplete CD19+/CD20+ B cells to treat refractory autoimmune diseases.
Autologous T cells are genetically engineered to express a dual-target chimeric antigen receptor recognizing CD19 and CD20 on B cells. Upon antigen engagement, the CAR T cells become activated and mediate cytotoxic killing of CD19+/CD20+ B-lineage cells, leading to B-cell depletion and suppression of autoantibody-driven immune responses.
YES
DIRECT
Dual-target CAR T cells bind CD20 on B cells, become activated, and kill the bound cells via perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis), depleting CD20+ cells.
Chimeric anti-CD20 monoclonal antibody given as 1000 mg IV infusion; depletes CD20+ B lymphocytes via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, reducing autoantibody production and pro-inflammatory signaling.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B lymphocytes and depletes them via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, reducing autoantibody production, antigen presentation, and pro-inflammatory signaling.
YES
DIRECT
Binds CD20 on B cells and triggers complement-dependent cytotoxicity and Fc-mediated ADCC; can also induce apoptosis of target cells.
Human IgG1 anti–PD-L1 monoclonal antibody checkpoint inhibitor that blocks PD-L1 from binding PD-1/CD80 to restore cytotoxic T-cell activity and can engage NK cell ADCC.
Human IgG1 monoclonal antibody against PD-L1 that blocks PD-L1 interaction with PD-1/CD80, releasing checkpoint-mediated inhibition to restore cytotoxic T-cell activity; its Fc can engage NK cells to mediate ADCC against PD-L1-expressing tumor cells.
YES
DIRECT
IgG1 Fc recruits NK cells via Fc gamma receptors to mediate ADCC against PD-L1–expressing cells; checkpoint blockade also restores CTL killing (indirect).
Human IgG1 anti–PD-L1 monoclonal antibody checkpoint inhibitor that blocks PD-L1 from binding PD-1/CD80 to restore cytotoxic T-cell activity and can engage NK cell ADCC.
Human IgG1 monoclonal antibody against PD-L1 that blocks PD-L1 interaction with PD-1/CD80, releasing checkpoint-mediated inhibition to restore cytotoxic T-cell activity; its Fc can engage NK cells to mediate ADCC against PD-L1-expressing tumor cells.
NO
INDIRECT
Avelumab engages CD16A (FcγRIIIA) on NK cells via its Fc to trigger ADCC against PD-L1–expressing targets; CD16A+ cells are effectors, not targets, and are not killed by the drug.
Autologous BCMA-directed CAR T-cell therapy (CART-ddBCMA) using a D-domain CAR binder; after cyclophosphamide/fludarabine lymphodepletion, infused CAR-T cells recognize BCMA on malignant plasma cells and induce T-cell activation and cytotoxic killing.
Autologous T cells are genetically engineered to express a BCMA-targeting chimeric antigen receptor (D-domain binder). Following cyclophosphamide/fludarabine lymphodepletion, the infused CAR T cells recognize BCMA on malignant plasma cells and trigger CAR-mediated T-cell activation, cytokine release, proliferation, and cytotoxic killing of BCMA-expressing myeloma cells.
YES
DIRECT
BCMA-directed CAR T cells bind BCMA on target cells, activate via CAR signaling, and kill through perforin/granzyme-mediated cytolysis and apoptosis (with cytokine release).