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.
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.
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.
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.
Autologous adoptive T-cell therapy consisting of ex vivo expanded, tumor‑reactive T lymphocytes harvested from tumor‑draining lymph nodes; administered after lymphodepletion to mediate antigen-specific cytotoxicity.
Autologous tumor‑reactive T lymphocytes harvested from tumor‑draining lymph nodes are expanded ex vivo and reinfused after lymphodepletion. These unengineered T cells recognize tumor antigens via their native TCRs in an MHC‑restricted manner, expand (with IL‑2 support), and mediate antigen‑specific cytotoxicity through perforin/granzyme release and cytokine production to eliminate tumor cells.
Infused tumor‑reactive T cells recognize the neoantigen peptide–HLA class I complex via native TCRs and directly kill target cells through cytolytic synapse formation with perforin/granzyme–mediated apoptosis (and Fas–FasL pathways).
Autologous adoptive T-cell therapy consisting of ex vivo expanded, tumor‑reactive T lymphocytes harvested from tumor‑draining lymph nodes; administered after lymphodepletion to mediate antigen-specific cytotoxicity.
Autologous tumor‑reactive T lymphocytes harvested from tumor‑draining lymph nodes are expanded ex vivo and reinfused after lymphodepletion. These unengineered T cells recognize tumor antigens via their native TCRs in an MHC‑restricted manner, expand (with IL‑2 support), and mediate antigen‑specific cytotoxicity through perforin/granzyme release and cytokine production to eliminate tumor cells.
Adoptively transferred tumor‑reactive T cells recognize the neoantigen peptide–HLA class II complex via their native TCRs and directly lyse the presenting cell through perforin/granzyme release (± Fas–FasL), with supportive cytokine effects.