Polyclonal antibody preparation that depletes T cells for GVHD prophylaxis.
Polyclonal IgG directed against multiple T-cell antigens that binds and depletes T cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and induction of apoptosis, leading to immunosuppression and GVHD prophylaxis.
NO
INDIRECT
Antithymocyte globulin targets multiple T‑cell antigens and depletes T cells via complement-dependent cytotoxicity, ADCC, and apoptosis; it is not directed against HLA-A, so HLA-A–expressing cells are not specifically killed.
Polyclonal antibody preparation that depletes T cells for GVHD prophylaxis.
Polyclonal IgG directed against multiple T-cell antigens that binds and depletes T cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and induction of apoptosis, leading to immunosuppression and GVHD prophylaxis.
NO
INDIRECT
Antithymocyte globulin binds multiple T‑cell antigens (not HLA class I) and depletes T cells via complement-dependent cytotoxicity, ADCC, and apoptosis; HLA-B expression is not the basis for killing.
Polyclonal antibody preparation that depletes T cells for GVHD prophylaxis.
Polyclonal IgG directed against multiple T-cell antigens that binds and depletes T cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and induction of apoptosis, leading to immunosuppression and GVHD prophylaxis.
NO
INDIRECT
Antithymocyte globulin binds multiple T‑cell surface antigens (not HLA-C) and depletes T cells via complement-dependent cytotoxicity, ADCC, and apoptosis; HLA-C–expressing cells are not directly targeted.
Polyclonal antibody preparation that depletes T cells for GVHD prophylaxis.
Polyclonal IgG directed against multiple T-cell antigens that binds and depletes T cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and induction of apoptosis, leading to immunosuppression and GVHD prophylaxis.
NO
INDIRECT
Antithymocyte globulin binds multiple T‑cell antigens and depletes T cells via complement-dependent cytotoxicity, ADCC, and apoptosis; it is not directed against HLA‑DR, so HLA‑DR–expressing cells are not directly killed via this target.
Autologous T cells genetically engineered to co-express a bispecific chimeric antigen receptor targeting CD19 and CD22, activating T-cell cytotoxicity against B-ALL blasts and reducing antigen-loss escape.
Autologous T cells are genetically engineered to co-express a bispecific chimeric antigen receptor that recognizes CD19 and CD22 on B-ALL cells. CAR engagement activates T-cell signaling, driving proliferation, cytokine release, and perforin/granzyme-mediated cytotoxicity, while dual targeting reduces antigen-loss escape compared with single-antigen CARs.
YES
DIRECT
Bispecific CAR T cells bind CD19 on target cells, triggering T-cell activation and perforin/granzyme-mediated cytolysis (and Fas/FasL apoptosis) of CD19-expressing cells.