Autologous peripheral blood T cells expanded and activated ex vivo to recognize MUC1 via TCR; infused intravenously as adoptive cellular immunotherapy to mediate tumor cell killing and cytokine release.
Autologous peripheral blood T cells are expanded ex vivo and enriched/activated for TCR-mediated recognition of MUC1 peptides presented on MHC. After infusion, these MUC1‑reactive T cells engage tumor cells, become activated, and mediate cytotoxicity via perforin/granzyme release and cytokine secretion (e.g., IFN-γ, TNF), leading to targeted tumor cell killing and immune amplification.
MUC1-specific T cells recognize MUC1 peptide–MHC on target cells and induce apoptosis via perforin/granzyme release (with possible Fas–FasL and cytokine-mediated effects).
Anti-CD79b antibody-drug conjugate that delivers the microtubule inhibitor MMAE to B cells, causing microtubule disruption and cell death.
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, leading to G2/M arrest and apoptotic death of malignant B cells.
ADC binds CD79b on B cells, is internalized, and releases MMAE via a protease-cleavable linker; MMAE inhibits tubulin polymerization, causing G2/M arrest and apoptotic cell death.
Chimeric anti-CD20 monoclonal antibody that depletes B cells via ADCC, CDC, and apoptosis.
Chimeric anti‑CD20 monoclonal antibody that binds CD20 on B cells and depletes them via antibody‑dependent cellular cytotoxicity (ADCC), complement‑dependent cytotoxicity (CDC), and induction of apoptosis.
Rituximab binds CD20 on B cells and induces killing via Fc-mediated ADCC by immune effectors, complement-dependent cytotoxicity, and CD20 cross-linking–induced apoptosis.
A subcutaneous bispecific (CD3xCD20) T-cell–engaging monoclonal antibody (GEN3013; DuoBody-CD3xCD20) that binds CD3 on T cells and CD20 on B cells to form an immune synapse and redirect cytotoxic T-cell killing of malignant B cells.
CD3xCD20 bispecific antibody that binds CD3 on T cells and CD20 on B cells to form an immune synapse, activating T-cell cytotoxicity (perforin/granzyme) and redirecting killing of CD20-positive malignant B cells in an MHC-independent manner.
Bispecific antibody links CD3 on T cells to CD20 on B cells, forming an immune synapse that activates T-cell cytotoxicity (perforin/granzyme) to kill CD20+ cells in an MHC-independent manner.
Rabbit polyclonal antilymphocyte globulin used for in vivo T-cell depletion to reduce graft-versus-host disease risk.
Rabbit polyclonal IgG against multiple human T‑cell surface antigens (e.g., CD2, CD3, CD4, CD8, HLA) that depletes T lymphocytes via complement-dependent cytotoxicity, Fc-mediated ADCC/phagocytosis, and apoptosis, producing in vivo T‑cell immunosuppression to reduce GVHD risk.
Polyclonal rabbit IgG in rATG binds CD7 on T cells; Fc activates complement (CDC) and engages Fcγ receptors for ADCC/phagocytosis, and can trigger apoptosis, depleting CD7+ cells.