Adoptive cellular therapy using patient-derived T cells engineered with a chimeric antigen receptor to target malignant hematologic cells (antigen not specified).
Autologous T cells are genetically engineered to express a chimeric antigen receptor that binds a tumor-associated surface antigen on malignant hematologic cells independent of MHC. Antigen engagement triggers CD3ζ signaling with costimulatory domains (e.g., CD28 or 4-1BB), leading to T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing, with potential in vivo expansion and persistence for ongoing antitumor activity.
CAR engagement on engineered T cells triggers activation and direct killing of antigen-expressing cells via perforin/granzyme-mediated cytolysis (and related apoptotic pathways).
Fc-enhanced anti-CTLA-4 monoclonal antibody that boosts T-cell priming and can deplete intratumoral regulatory T cells via ADCC.
Fc-engineered anti-CTLA-4 IgG1 monoclonal antibody that blocks CTLA-4 to relieve inhibitory signaling and enhance T-cell priming/activation; enhanced Fc effector function enables ADCC-mediated depletion of intratumoral regulatory T cells and increases antibody stability/half-life.
The Fc-engineered IgG1 binds CTLA-4 on target cells (e.g., intratumoral Tregs) and engages FcγR-expressing effector cells to mediate ADCC/ADCP, depleting CTLA-4–positive cells.
Polyclonal anti-T cell immunoglobulin used for T-lymphocyte depletion to reduce alloimmune responses.
Polyclonal anti–T‑cell immunoglobulin that binds multiple T‑lymphocyte surface antigens (e.g., CD2, CD3, CD4, CD8, CD25, HLA), triggering complement-dependent cytotoxicity, antibody‑dependent cellular cytotoxicity, and apoptosis, resulting in rapid T‑cell depletion and suppression of alloimmune responses.
ATG binds CD2 on T cells and induces complement-dependent cytotoxicity and Fc-mediated ADCC, with additional apoptosis, leading to direct T-cell depletion.
Polyclonal anti-T cell immunoglobulin used for T-lymphocyte depletion to reduce alloimmune responses.
Polyclonal anti–T‑cell immunoglobulin that binds multiple T‑lymphocyte surface antigens (e.g., CD2, CD3, CD4, CD8, CD25, HLA), triggering complement-dependent cytotoxicity, antibody‑dependent cellular cytotoxicity, and apoptosis, resulting in rapid T‑cell depletion and suppression of alloimmune responses.
ATG antibodies bind CD4 on T cells and trigger complement-dependent lysis and Fc-mediated ADCC, and can induce apoptosis, leading to direct depletion of CD4+ cells.