Polyclonal anti-T-cell antibody used in conditioning for T-cell depletion prior to HSCT.
Polyclonal anti-T-cell immunoglobulin that binds multiple T-cell surface antigens (e.g., CD2, CD3, CD4, CD8, HLA-DR), depleting T lymphocytes via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, resulting in profound T-cell immunosuppression and reduction of alloreactivity before HSCT.
YES
DIRECT
ATG antibodies bind CD8 (including CD8 beta) on T cells and trigger complement-dependent cytotoxicity, FcγR-mediated ADCC, and apoptosis, depleting CD8+ T cells.
Polyclonal anti-T-cell antibody used in conditioning for T-cell depletion prior to HSCT.
Polyclonal anti-T-cell immunoglobulin that binds multiple T-cell surface antigens (e.g., CD2, CD3, CD4, CD8, HLA-DR), depleting T lymphocytes via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, resulting in profound T-cell immunosuppression and reduction of alloreactivity before HSCT.
YES
DIRECT
Polyclonal antibodies in ATG bind HLA-DR on the cell surface, triggering complement-dependent lysis, Fc-mediated ADCC/phagocytosis, and apoptosis, leading to depletion of HLA-DR–expressing cells.
Polyclonal anti-T-cell antibody used in conditioning for T-cell depletion prior to HSCT.
Polyclonal anti-T-cell immunoglobulin that binds multiple T-cell surface antigens (e.g., CD2, CD3, CD4, CD8, HLA-DR), depleting T lymphocytes via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, resulting in profound T-cell immunosuppression and reduction of alloreactivity before HSCT.
YES
DIRECT
Polyclonal antibodies in ATG bind HLA-DR on target cells, triggering complement-dependent lysis and Fc-mediated ADCC/phagocytosis, leading to apoptosis/lysis.
Anti-CD20 monoclonal antibody used to deplete B cells and prevent EBV-associated PTLD.
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; used to reduce CD20+ B cells and prevent EBV-associated PTLD.
YES
DIRECT
Rituximab binds CD20 on B cells and triggers complement-dependent cytotoxicity (MAC lysis), antibody-dependent cellular cytotoxicity via FcγR-bearing effector cells (e.g., NK cells, macrophages), and can induce apoptosis upon CD20 crosslinking.
Autologous CD19/CD20-directed chimeric antigen receptor (CAR) T-cell therapy; patient T cells are genetically engineered to express CARs targeting CD19 and CD20 on B cells to mediate cytotoxic killing of lymphoma cells.
Autologous T cells are genetically engineered to express a chimeric antigen receptor recognizing CD19 and CD20 on B cells; antigen binding activates CAR signaling to expand and activate the T cells, leading to cytokine release and perforin/granzyme-mediated cytotoxic killing of malignant B cells, with on-target depletion of normal B cells.
YES
DIRECT
CAR T cells engineered to target CD19 bind the antigen and, upon CAR signaling, kill CD19+ cells via perforin/granzyme release (and death receptor pathways), leading to apoptosis/lysis.