Autologous second-generation anti-CD19 chimeric antigen receptor T-cell therapy using an HI19α-derived scFv with 4-1BB and CD3ζ signaling domains to target and eliminate CD19+ B cells/plasmablasts, aiming to reduce pathogenic autoantibody production in AIHA/Evans syndrome.
Autologous T cells are genetically engineered to express an anti‑CD19 chimeric antigen receptor (HI19a-derived scFv with 4-1BB costimulatory and CD3zeta signaling domains). Binding to CD19 on B cells and plasmablasts activates the CAR T cells, leading to expansion and cytotoxic elimination of CD19+ cells, thereby depleting pathogenic B-cell populations and reducing autoantibody production in AIHA/Evans syndrome.
Anti-CD19 CAR T cells bind CD19 on B cells, become activated, and kill targets via T cell cytotoxic mechanisms (immune synapse formation, perforin/granzyme release and Fas–FasL–mediated apoptosis).
Anti-CD20 monoclonal antibody that depletes B cells via ADCC, CDC, and apoptosis.
Chimeric anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and depletes malignant and normal B cells via Fc-mediated ADCC and phagocytosis, complement-dependent cytotoxicity, and direct induction of apoptosis.
Binds CD20 on B cells and induces Fc-mediated ADCC/phagocytosis by NK cells/macrophages, complement-dependent cytotoxicity, and direct apoptotic signaling.
CD20xCD3 bispecific T-cell–engaging antibody that recruits and activates T cells via CD3 to kill CD20+ B cells.
CD20xCD3 bispecific antibody that simultaneously binds CD20 on B cells and CD3 on T cells, crosslinking them to activate T-cell signaling and cytotoxicity, leading to targeted lysis of CD20-positive malignant B cells.
Glofitamab bridges CD3+ T cells to CD20+ cells, activating T-cell cytotoxicity that kills the CD20-expressing cells via perforin/granzyme-mediated lysis (and related effector pathways).
Adoptive γδ T‑cell therapy using Vγ9Vδ2 T cells expanded from healthy donors and administered intraventricularly/intracavitary via an Ommaya reservoir. These innate‑like cytotoxic lymphocytes recognize tumor phosphoantigens via BTN3A1/BTN2A1 independent of MHC, triggering perforin/granzyme‑mediated killing and cytokine release; they can also respond via NKG2D and mediate ADCC.
Allogeneic Vγ9Vδ2 T cells recognize tumor-derived phosphoantigens generated by dysregulated mevalonate metabolism via BTN3A1/BTN2A1 in an MHC-independent manner, triggering perforin/granzyme-mediated cytotoxicity and cytokine release. They also respond to stress ligands through NKG2D and can mediate ADCC.
Vγ9Vδ2 T cells use NKG2D to recognize ULBP4 on target cells, triggering activation and perforin/granzyme-mediated cytolysis.
Anti-CD79b antibody–drug conjugate that delivers MMAE to CD79b+ B cells, disrupting microtubules and inducing apoptosis.
Anti-CD79b monoclonal antibody linked via a protease-cleavable linker to the microtubule inhibitor MMAE. After binding CD79b on B cells and internalization, MMAE is released to inhibit tubulin polymerization, causing G2/M arrest and apoptosis of malignant B cells.
Anti‑CD79b ADC binds CD79b on B cells, is internalized, and releases MMAE after linker cleavage; MMAE inhibits tubulin polymerization, causing G2/M arrest and apoptosis of the target cells.