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.
YES
DIRECT
ATG contains antibodies that bind CD4 on T cells, triggering complement-dependent lysis and Fc-mediated ADCC by NK/macrophages, with additional apoptosis induction, depleting CD4+ cells.
Autologous adoptive cell therapy using patient-derived tumor-infiltrating T cells expanded ex vivo to recognize and kill cancer cells.
Autologous tumor-infiltrating T cells are isolated from the patient’s tumor, expanded ex vivo, and reinfused after lymphodepletion. These unengineered T cells recognize patient-specific tumor antigens via their native TCRs and mediate MHC-restricted cytotoxicity (perforin/granzyme) and cytokine-driven immune responses within the tumor, resulting in direct killing of cancer cells; IL-2 is often provided to support in vivo expansion and persistence.
YES
DIRECT
TILs recognize the neoantigen peptide–HLA class I complex via native TCRs and directly kill target cells through MHC-restricted cytotoxicity (perforin/granzyme release and Fas–FasL–mediated apoptosis).
Autologous adoptive cell therapy using patient-derived tumor-infiltrating T cells expanded ex vivo to recognize and kill cancer cells.
Autologous tumor-infiltrating T cells are isolated from the patient’s tumor, expanded ex vivo, and reinfused after lymphodepletion. These unengineered T cells recognize patient-specific tumor antigens via their native TCRs and mediate MHC-restricted cytotoxicity (perforin/granzyme) and cytokine-driven immune responses within the tumor, resulting in direct killing of cancer cells; IL-2 is often provided to support in vivo expansion and persistence.
YES
DIRECT
TILs contain tumor‑reactive CD4+ T cells whose native TCRs recognize the peptide–HLA class II complex on target cells, triggering MHC II–restricted cytotoxicity via perforin/granzyme release and Fas–FasL–mediated apoptosis.
A human IgG1 monoclonal antibody targeting OX40 (CD134) on activated T cells; blocks OX40–OX40L costimulation and can deplete OX40+ T cells to reduce type‑2 inflammation.
Human IgG1 monoclonal antibody that binds OX40 (CD134) on activated T cells, blocking OX40–OX40L costimulatory signaling and, via Fc effector functions, can deplete OX40+ T cells, reducing type‑2 (Th2) inflammation.
YES
DIRECT
After binding OX40 on activated T cells, the IgG1 Fc engages effector mechanisms (ADCC/ADCP and possibly complement), leading to depletion/lysis of OX40+ cells.
Autologous, gene‑modified CD19‑directed CAR T‑cell therapy (CARTEYVA). Patient T cells are engineered to express an anti‑CD19 chimeric antigen receptor with 4‑1BB costimulatory and CD3ζ signaling domains; upon binding CD19 on B‑cell lymphomas, the CAR T cells expand and mediate perforin/granzyme‑dependent cytotoxicity, leading to B‑cell depletion.
Autologous T cells are gene-modified to express an anti-CD19 chimeric antigen receptor with 4-1BB costimulatory and CD3ζ signaling domains; upon binding CD19 on malignant B cells, the CAR T cells activate, expand, and kill targets via perforin/granzyme-mediated cytotoxicity, depleting CD19-positive B-cell lymphomas.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 on target cells, activate, and kill via perforin/granzyme-mediated cytotoxicity leading to apoptosis/lysis.