Autologous monocyte-derived dendritic cell vaccine loaded ex vivo with Epstein–Barr virus antigens to present peptides on MHC I/II and prime/expand EBV-specific CD8+ and CD4+ T cells, promoting a Th1 response and cytotoxic killing of EBV-positive malignant cells.
Autologous monocyte-derived dendritic cells are loaded ex vivo with EBV antigens and, upon administration, present EBV peptides on MHC I/II to prime and expand EBV-specific CD8+ cytotoxic and CD4+ helper T cells, promoting a Th1 response and cytolytic killing of EBV-positive malignant cells.
YES
INDIRECT
The DC vaccine primes/expands EBV-specific CD8+ T cells, which recognize EBV peptide–HLA I complexes on target cells and kill them via perforin/granzyme (and Fas–FasL) cytotoxicity.
Autologous monocyte-derived dendritic cell vaccine loaded ex vivo with Epstein–Barr virus antigens to present peptides on MHC I/II and prime/expand EBV-specific CD8+ and CD4+ T cells, promoting a Th1 response and cytotoxic killing of EBV-positive malignant cells.
Autologous monocyte-derived dendritic cells are loaded ex vivo with EBV antigens and, upon administration, present EBV peptides on MHC I/II to prime and expand EBV-specific CD8+ cytotoxic and CD4+ helper T cells, promoting a Th1 response and cytolytic killing of EBV-positive malignant cells.
YES
INDIRECT
The DC vaccine primes and expands EBV-specific T cells; these T cells recognize EBV peptides presented on HLA (including class II) and kill EBV+ cells via perforin/granzyme and Fas–FasL pathways. The vaccine itself does not directly kill cells.
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.
NO
INDIRECT
ATG binds multiple T‑cell surface antigens (e.g., CD2, CD3, CD4, CD8) and depletes T cells via complement-dependent cytotoxicity and Fc-mediated ADCC/apoptosis; it is not directed against HLA‑B, so HLA‑B expression alone is not a cytotoxic target.
Afucosylated anti–IL-5Rα monoclonal antibody that depletes eosinophils (and basophils) via antibody-dependent cellular cytotoxicity (ADCC).
Afucosylated anti-IL-5Ralpha monoclonal antibody that binds IL-5 receptor alpha on eosinophils and basophils, triggering strong ADCC to deplete these cells and thereby suppress IL-5 signaling and type 2 inflammation.
YES
DIRECT
Benralizumab binds IL-5Rα on eosinophils/basophils and, via its afucosylated Fc, strongly engages FcγRIIIa on NK cells to trigger ADCC (perforin/granzyme-mediated killing), depleting IL-5Rα+ cells.
Afucosylated anti–IL-5Rα monoclonal antibody that depletes eosinophils (and basophils) via antibody-dependent cellular cytotoxicity (ADCC).
Afucosylated anti-IL-5Ralpha monoclonal antibody that binds IL-5 receptor alpha on eosinophils and basophils, triggering strong ADCC to deplete these cells and thereby suppress IL-5 signaling and type 2 inflammation.
NO
INDIRECT
Benralizumab’s afucosylated Fc engages CD16a on NK cells to induce ADCC against IL-5Rα–expressing eosinophils/basophils; CD16a+ cells are effectors, not killed.