Autologous CD7-directed chimeric antigen receptor (CAR) T-cell therapy. Patient T cells are engineered to express a CD7-targeted CAR (CD3ζ with costimulation); upon CD7 engagement, CAR signaling activates and expands T cells to kill CD7+ malignant cells via perforin/granzyme and cytokine-mediated cytotoxicity in r/r T-ALL, lymphoblastic lymphoma, and CD7-positive AML.
Autologous T cells are genetically engineered to express a CD7-directed chimeric antigen receptor (with CD3ζ signaling and costimulatory domains). Upon binding CD7 on malignant cells, CAR activation drives T‑cell activation, expansion, and cytotoxic killing via perforin/granzyme release and cytokine-mediated mechanisms, depleting CD7+ leukemic/lymphoma cells.
YES
DIRECT
CD7-targeted CAR T cells bind CD7 on target cells and kill them via CAR-activated cytotoxicity, primarily perforin/granzyme-mediated lysis (with cytokine/Fas–FasL contributions).
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 EBNA1-derived peptides presented by HLA on target cells via their native TCRs and kill them through perforin/granzyme (and Fas/FasL)–mediated 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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
HLA-restricted TCR recognition of EBNA3C-derived peptides on infected/malignant cells triggers CTL degranulation with perforin/granzymes (and Fas/FasL), inducing apoptosis.