Patient-derived tumor-infiltrating lymphocytes expanded ex vivo and infused after preparative chemotherapy; mediate tumor antigen-specific cytotoxicity via TCR recognition to repopulate with highly tumor-reactive T cells.
Autologous tumor-infiltrating lymphocytes expanded ex vivo are infused after lymphodepleting chemotherapy; they recognize tumor antigens via native TCRs and mediate antigen-specific cytotoxicity, persisting and expanding in vivo to repopulate with highly tumor-reactive T cells.
TILs recognize the tumor peptide–HLA-DP complex via native TCRs and directly kill the presenting cell through perforin/granzyme release and Fas–FasL–mediated apoptosis.
Monoclonal antibody against CD20 that depletes pre-B and mature B cells to reduce ANCA production.
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, thereby reducing ANCA production.
Binds CD20 on B cells and triggers complement-dependent cytotoxicity and Fc-mediated effector killing (ADCC/ADCP), with additional apoptosis upon crosslinking.
Human IgG1 monoclonal antibody targeting CD38; depletes CD38+ immune cells (plasma cells, B cells, T cells, dendritic cells, macrophages) via ADCC, CDC, ADCP, and apoptosis to reduce pathogenic auto/alloantibody production.
Human IgG1 monoclonal antibody targeting CD38 that depletes CD38-expressing cells (plasma cells, selected B/T cells, myeloid and tumor cells) by inducing antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, antibody-dependent cellular phagocytosis, and apoptosis, thereby reducing pathogenic antibody production.
Daratumumab binds CD38 on target cells; its Fc domain recruits immune effectors to induce ADCC (NK cells), CDC (complement), ADCP (macrophages), and can trigger apoptosis of CD38+ cells.
A bispecific T-cell engager (BiTE) antibody construct that binds CD19 on B-ALL cells and CD3 on T cells to redirect cytotoxic T cells to kill CD19+ leukemic cells; administered IV in conditioning.
A bispecific anti-CD19/anti-CD3 antibody (BiTE) that simultaneously binds CD19 on B cells and CD3 on T cells, bringing them into proximity to activate T cells and mediate cytotoxic killing of CD19-positive leukemic cells.
Blinatumomab bridges CD19 on target cells to CD3 on T cells, activating T cells to kill CD19+ cells via perforin/granzyme-mediated cytotoxicity (immunologic synapse formation).
Autologous, genetically modified T lymphocytes engineered to express a chimeric antigen receptor targeting a B-cell surface antigen; CAR signaling (CD3ζ with costimulatory domains) activates T cells to proliferate, release cytokines, and kill malignant B cells.
Autologous T lymphocytes are genetically engineered to express a chimeric antigen receptor that binds a B‑cell surface antigen. Antigen engagement triggers CAR signaling (CD3ζ with costimulatory domains), activating the T cells to expand, release cytokines, and kill malignant B cells via cytotoxic mechanisms (e.g., perforin/granzyme‑mediated apoptosis).
CAR binding to the B‑cell surface antigen activates the engineered T cells, which kill target cells via perforin/granzyme-mediated apoptosis (and death-receptor pathways).