Anti-CD20 monoclonal antibody that depletes CD20-positive B-cell blasts via complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and B-lymphoblasts, triggering complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity to deplete CD20-positive cells.
YES
DIRECT
Rituximab binds CD20 on B cells and triggers complement-dependent cytotoxicity and Fc-mediated effector killing (ADCC/ADCP), directly eliminating CD20+ cells.
Autologous, gene-modified CAR T-cell therapy engineered to co-target CD19 and BCMA to deplete CD19+ B cells and BCMA+ plasmablasts/long-lived plasma cells, aiming to reset humoral immunity and reduce autoantibody production in lupus nephritis and IgG4-related disease.
Autologous gene‑modified T cells expressing dual CARs targeting CD19 and BCMA selectively recognize and kill CD19+ B cells and BCMA+ plasmablasts/long‑lived plasma cells, depleting pathogenic B‑lineage compartments to reduce autoantibody production and reset humoral immunity in autoimmune disease.
YES
DIRECT
CD19-directed CAR T cells bind CD19 on target cells and kill them via T cell cytotoxicity (immune synapse formation, perforin/granzyme release, and apoptosis pathways such as Fas-FasL).
Autologous, gene-modified CAR T-cell therapy engineered to co-target CD19 and BCMA to deplete CD19+ B cells and BCMA+ plasmablasts/long-lived plasma cells, aiming to reset humoral immunity and reduce autoantibody production in lupus nephritis and IgG4-related disease.
Autologous gene‑modified T cells expressing dual CARs targeting CD19 and BCMA selectively recognize and kill CD19+ B cells and BCMA+ plasmablasts/long‑lived plasma cells, depleting pathogenic B‑lineage compartments to reduce autoantibody production and reset humoral immunity in autoimmune disease.
YES
DIRECT
Anti-BCMA CAR T cells recognize BCMA on target cells and directly kill them via T-cell cytotoxic mechanisms (perforin/granzyme and Fas–FasL–mediated apoptosis).
Autologous tumor-infiltrating lymphocyte (TIL) therapy expanded ex vivo and reinfused to mediate patient-specific, TCR-dependent antitumor cytotoxicity.
Autologous tumor-infiltrating lymphocytes expanded ex vivo are reinfused to recognize patient-specific tumor antigens via their native T-cell receptors and kill tumor cells through perforin/granzyme-mediated cytotoxicity and cytokine release, often supported by IL-2 to enhance expansion and persistence.
YES
DIRECT
Autologous TILs recognize the patient-specific neoantigen peptide presented on MHC via their native TCRs and directly kill the tumor cell through perforin/granzyme release (with possible Fas–FasL and cytokine-mediated effects).
Autologous tumor-infiltrating lymphocyte (TIL) therapy expanded ex vivo and reinfused to mediate patient-specific, TCR-dependent antitumor cytotoxicity.
Autologous tumor-infiltrating lymphocytes expanded ex vivo are reinfused to recognize patient-specific tumor antigens via their native T-cell receptors and kill tumor cells through perforin/granzyme-mediated cytotoxicity and cytokine release, often supported by IL-2 to enhance expansion and persistence.
YES
DIRECT
Autologous TILs recognize HPV E6 peptide presented on HLA by tumor cells via their native TCRs and induce perforin/granzyme-mediated apoptosis (with possible Fas/FasL and cytokine-mediated cytotoxicity).