Donor-derived, ex vivo–expanded polyclonal CD8+ and CD4+ T cells specific for Epstein–Barr virus antigens (e.g., EBNA, LMP) administered post-transplant as adoptive cellular immunotherapy to restore antiviral immunity and eliminate EBV-infected/malignant cells.
Donor-derived, ex vivo–expanded EBV-specific CD8+/CD4+ T cells use their native, HLA-restricted TCRs to recognize EBV antigens (e.g., EBNA, LMP) on infected or malignant cells and eliminate them via perforin/granzyme cytotoxicity and Th1 cytokines, restoring antiviral immunity and controlling EBV-driven lymphoproliferation with low GVHD risk.
HLA-restricted TCR recognition of EBNA3A-derived peptides on target cells triggers CTL killing via perforin/granzyme–mediated apoptosis (± Fas/FasL).
Donor-derived, ex vivo–expanded polyclonal CD8+ and CD4+ T cells specific for Epstein–Barr virus antigens (e.g., EBNA, LMP) administered post-transplant as adoptive cellular immunotherapy to restore antiviral immunity and eliminate EBV-infected/malignant cells.
Donor-derived, ex vivo–expanded EBV-specific CD8+/CD4+ T cells use their native, HLA-restricted TCRs to recognize EBV antigens (e.g., EBNA, LMP) on infected or malignant cells and eliminate them via perforin/granzyme cytotoxicity and Th1 cytokines, restoring antiviral immunity and controlling EBV-driven lymphoproliferation with low GVHD risk.
HLA-restricted TCR recognition of EBNA3B-derived peptides on target cells triggers CD8+ EBV-specific T-cell killing via perforin/granzyme (and Fas–FasL) cytotoxicity.
Donor-derived, ex vivo–expanded polyclonal CD8+ and CD4+ T cells specific for Epstein–Barr virus antigens (e.g., EBNA, LMP) administered post-transplant as adoptive cellular immunotherapy to restore antiviral immunity and eliminate EBV-infected/malignant cells.
Donor-derived, ex vivo–expanded EBV-specific CD8+/CD4+ T cells use their native, HLA-restricted TCRs to recognize EBV antigens (e.g., EBNA, LMP) on infected or malignant cells and eliminate them via perforin/granzyme cytotoxicity and Th1 cytokines, restoring antiviral immunity and controlling EBV-driven lymphoproliferation with low GVHD risk.
HLA-restricted TCR recognition of EBNA3C-derived peptides on infected/malignant cells triggers CTL degranulation with perforin/granzymes (and Fas/FasL), inducing apoptosis.
Donor-derived, ex vivo–expanded polyclonal CD8+ and CD4+ T cells specific for Epstein–Barr virus antigens (e.g., EBNA, LMP) administered post-transplant as adoptive cellular immunotherapy to restore antiviral immunity and eliminate EBV-infected/malignant cells.
Donor-derived, ex vivo–expanded EBV-specific CD8+/CD4+ T cells use their native, HLA-restricted TCRs to recognize EBV antigens (e.g., EBNA, LMP) on infected or malignant cells and eliminate them via perforin/granzyme cytotoxicity and Th1 cytokines, restoring antiviral immunity and controlling EBV-driven lymphoproliferation with low GVHD risk.
EBV-specific T cells recognize LMP1-derived peptides presented on HLA via their native TCRs and directly kill target cells through perforin/granzyme release (and Fas–FasL apoptosis).
An intravenous, glycoengineered type II anti-CD20 humanized IgG1 monoclonal antibody that induces B-cell death and immune effector killing (ADCC/ADCP; some CDC).
Humanized, glycoengineered type II anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and triggers direct B‑cell death and Fc-mediated effector killing (enhanced ADCC/ADCP with limited CDC) via increased affinity of its afucosylated Fc for FcgammaRIIIa.
Obinutuzumab binds CD20 on B cells, inducing direct type II anti-CD20 cell death and engaging immune effectors via its afucosylated Fc to drive ADCC and ADCP (with limited CDC).