Gene-modified cellular immunotherapy consisting of gamma-delta T lymphocytes engineered to express a CD19-specific chimeric antigen receptor; administered by IV infusion to deplete CD19+ B-lineage cells and suppress B cell–mediated autoimmunity.
Gamma-delta T lymphocytes engineered to express a CD19-specific chimeric antigen receptor bind CD19 on B-lineage cells, triggering T-cell activation and cytotoxicity (perforin/granzyme and inflammatory cytokines) to deplete CD19+ B cells and suppress B cell–mediated autoimmunity.
CD19 CAR γδ T cells bind CD19 on target cells, become activated, and kill via perforin/granzyme-mediated cytolysis (with supportive inflammatory cytokines).
A fully human type I anti-CD20 monoclonal antibody administered subcutaneously that depletes CD20+ B cells via complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity, reducing B-cell antigen presentation and autoantibody production in multiple sclerosis.
Fully human type I anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes them via complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity, reducing B-cell antigen presentation and autoantibody production.
Binds CD20 on B cells and induces complement-dependent cytotoxicity and Fc-mediated effector killing (ADCC/ADCP), leading to lysis/depletion of CD20+ cells.
Humanized IgG1 monoclonal antibody targeting MUC1 on cancer cells; engages Fcγ receptor–bearing effector cells (e.g., NK cells/macrophages) to mediate ADCC/CDC.
Humanized IgG1 monoclonal antibody targeting MUC1 on tumor cells; engages Fcγ receptor–bearing effector cells (e.g., NK cells, macrophages) to induce antibody‑dependent cellular cytotoxicity and complement‑dependent cytotoxicity, resulting in tumor cell killing.
Antibody binds MUC1 on tumor cells and engages FcγR-bearing effector cells to mediate ADCC and activates complement for CDC, leading to lysis of MUC1-expressing cells.
Intravenous anti-PD-L1 monoclonal antibody immunotherapy that blocks PD-L1 to disrupt the PD-1/PD-L1 checkpoint and restore cytotoxic T-cell antitumor activity.
Human IgG1 anti-PD-L1 monoclonal antibody that binds PD-L1 and blocks its interaction with PD-1, inhibiting checkpoint signaling to restore cytotoxic T-cell activity; also capable of inducing antibody-dependent cellular cytotoxicity against PD-L1-expressing tumor cells.
IgG1 Fc mediates ADCC by NK cells (and other FcγR+ effectors) against PD-L1–expressing cells; checkpoint blockade also restores T-cell killing (indirect).
Allogeneic donor-derived T cells genetically modified via lentiviral transduction to express a CD33-specific CAR with a CD8 hinge, 4-1BB costimulatory, and CD3ζ signaling domains, including a truncated EGFR (EGFRt) safety tag for potential ablation; designed to target CD33+ AML cells.
Allogeneic T cells are lentivirally engineered to express a CD33-specific CAR with 4-1BB costimulation and CD3ζ signaling. Upon binding CD33 on AML cells, the CAR activates T-cell cytotoxicity and proliferation, leading to targeted lysis of CD33+ cells; a truncated EGFR tag enables cetuximab-mediated ablation as a safety switch.
CAR binding to CD33 activates CD3ζ/4-1BB signaling in the engineered T cells, triggering targeted lysis of CD33+ cells via perforin/granzyme-mediated cytotoxicity (and Fas/FasL apoptosis).