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.
YES
DIRECT
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.
YES
DIRECT
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).
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.
YES
DIRECT
Native TCRs on EBV-specific T cells recognize LMP2A-derived peptides presented on HLA and induce apoptosis of target cells via perforin/granzyme (± 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.
YES
DIRECT
Native, HLA-restricted EBV-specific T cells recognize LMP2B-derived peptides on MHC and induce perforin/granzyme-mediated apoptosis of the target cells (with Th1 cytokine support).
An anti-CD30 antibody–drug conjugate consisting of a CD30-directed IgG1 monoclonal antibody linked to the cytotoxic payload monomethyl auristatin E (MMAE). It binds CD30 on tumor cells, is internalized, and releases MMAE intracellularly to inhibit microtubules, leading to G2/M arrest and apoptosis; may also mediate ADCC and bystander cytotoxicity.
CD30-directed IgG1 antibody-drug conjugate; binds CD30 on tumor cells and is internalized. Lysosomal proteases cleave the valine-citrulline linker to release MMAE, which inhibits tubulin polymerization, causing G2/M cell-cycle arrest and apoptosis; may also elicit ADCC and bystander cytotoxicity.
YES
DIRECT
An anti-CD30 ADC binds CD30, is internalized, and releases MMAE intracellularly to inhibit microtubules, causing G2/M arrest and apoptosis; can also mediate ADCC and bystander killing.