Polyclonal antibody preparation that depletes T lymphocytes for induction immunosuppression.
Polyclonal anti–T-lymphocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity and Fc-mediated ADCC, with additional T-cell apoptosis and functional inhibition, producing potent immunosuppression.
ATG binds CD28 on T cells and depletes them via complement-dependent cytotoxicity and Fc-mediated ADCC, with additional apoptosis induction.
Chimeric anti-CD20 monoclonal antibody immunotherapy that binds CD20 on B cells and depletes malignant cells via antibody-dependent cellular cytotoxicity, complement-mediated cytotoxicity, and apoptosis; administered intralesionally in this trial.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive malignant B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis; in this trial administered intralesionally for local effect.
Rituximab binds CD20 on B cells and kills them via Fc-mediated ADCC by immune effector cells, complement-dependent cytotoxicity, and antibody-induced apoptosis.
Partial HLA-matched multivirus-specific cytotoxic T lymphocytes administered by IV infusion to restore antiviral cellular immunity after allo-HSCT by HLA-restricted TCR recognition of CMV/EBV antigens and perforin/granzyme-mediated cytolysis.
Adoptive transfer of partial HLA-matched virus-specific cytotoxic T lymphocytes that use their endogenous, HLA-restricted TCRs to recognize CMV/EBV peptides on infected cells, expand in vivo, and mediate killing via perforin/granzyme and cytokine release, thereby clearing infected cells and restoring antiviral cellular immunity after allo-HSCT.
Adoptively transferred CMV-specific T cells recognize CMV peptide–HLA complexes via their endogenous TCRs and directly kill infected cells through perforin/granzyme-mediated cytolysis (with cytokine support).
Partial HLA-matched multivirus-specific cytotoxic T lymphocytes administered by IV infusion to restore antiviral cellular immunity after allo-HSCT by HLA-restricted TCR recognition of CMV/EBV antigens and perforin/granzyme-mediated cytolysis.
Adoptive transfer of partial HLA-matched virus-specific cytotoxic T lymphocytes that use their endogenous, HLA-restricted TCRs to recognize CMV/EBV peptides on infected cells, expand in vivo, and mediate killing via perforin/granzyme and cytokine release, thereby clearing infected cells and restoring antiviral cellular immunity after allo-HSCT.
Virus-specific T cells recognize EBV peptide–HLA complexes via their endogenous TCRs and kill the presenting cells by perforin/granzyme–mediated apoptosis (with possible Fas–FasL and cytokine-mediated effects).
A half-life–extended bispecific T‑cell engager (BiTE) antibody construct that binds DLL3 on tumor cells and CD3 on T cells to redirect cytotoxic T cells, inducing tumor cell lysis and cytokine release; administered subcutaneously.
A half-life–extended bispecific T-cell engager antibody that binds DLL3 on tumor cells and CD3 on T cells, redirecting and activating cytotoxic T lymphocytes to form an immune synapse and induce perforin/granzyme-mediated lysis and cytokine release against DLL3-expressing tumor cells.
Tarlatamab bridges CD3+ T cells to DLL3-expressing cells, forming an immune synapse and activating CTLs to kill target cells via perforin/granzyme-mediated cytolysis and apoptosis.