Allogeneic T cells engineered with an anti-CD7 chimeric antigen receptor to selectively eliminate CD7-expressing lymphocytes (T cells and some NK cells), providing deep lymphodepletion and immunosuppression prior to transplant in severe aplastic anemia.
Allogeneic donor T cells are genetically engineered to express an anti-CD7 chimeric antigen receptor. Upon binding CD7 on T cells (and some NK cells), the CAR redirects cytotoxic killing to deplete CD7-positive lymphocytes, inducing deep lymphodepletion and immunosuppression to remove autoreactive T cells and facilitate engraftment prior to allo-HSCT in severe aplastic anemia.
YES
DIRECT
Anti-CD7 CAR-T cells bind CD7 on target lymphocytes, become activated, and kill via cytolytic degranulation (perforin/granzyme) and death-receptor pathways (e.g., Fas/FasL), inducing apoptosis of CD7+ cells.
Allogeneic unmodified invariant natural killer T (iNKT) cell therapy; iNKT cells recognize glycolipid antigens via CD1d, secrete Th1 cytokines, and activate NK cells, CD8 T cells, and macrophages to kill tumor and remodel the tumor microenvironment.
Allogeneic, unmodified invariant NKT cells that recognize CD1d-presented glycolipid antigens and stress ligands via invariant TCR and NKG2D, secrete Th1 cytokines (e.g., IFN-γ), activate NK cells, CD8 T cells, and macrophages, and directly lyse tumor cells to remodel the tumor microenvironment.
YES
DIRECT
iNKT cells recognize the CD1d–glycolipid complex via their invariant TCR and directly kill the presenting cell by releasing cytotoxic granules (perforin/granzyme) and engaging death-receptor pathways.
Allogeneic unmodified invariant natural killer T (iNKT) cell therapy; iNKT cells recognize glycolipid antigens via CD1d, secrete Th1 cytokines, and activate NK cells, CD8 T cells, and macrophages to kill tumor and remodel the tumor microenvironment.
Allogeneic, unmodified invariant NKT cells that recognize CD1d-presented glycolipid antigens and stress ligands via invariant TCR and NKG2D, secrete Th1 cytokines (e.g., IFN-γ), activate NK cells, CD8 T cells, and macrophages, and directly lyse tumor cells to remodel the tumor microenvironment.
YES
DIRECT
iNKT cells in AgenT-797 express NKG2D, which binds MICA on target cells and triggers direct cytotoxic degranulation (perforin/granzymes) leading to apoptosis; Th1 cytokines further enhance killing.
Allogeneic unmodified invariant natural killer T (iNKT) cell therapy; iNKT cells recognize glycolipid antigens via CD1d, secrete Th1 cytokines, and activate NK cells, CD8 T cells, and macrophages to kill tumor and remodel the tumor microenvironment.
Allogeneic, unmodified invariant NKT cells that recognize CD1d-presented glycolipid antigens and stress ligands via invariant TCR and NKG2D, secrete Th1 cytokines (e.g., IFN-γ), activate NK cells, CD8 T cells, and macrophages, and directly lyse tumor cells to remodel the tumor microenvironment.
YES
DIRECT
iNKT cells in AgenT-797 express NKG2D, which binds MICB on target cells, triggering direct cytotoxicity (perforin/granzyme-mediated lysis and death receptor pathways).
Allogeneic unmodified invariant natural killer T (iNKT) cell therapy; iNKT cells recognize glycolipid antigens via CD1d, secrete Th1 cytokines, and activate NK cells, CD8 T cells, and macrophages to kill tumor and remodel the tumor microenvironment.
Allogeneic, unmodified invariant NKT cells that recognize CD1d-presented glycolipid antigens and stress ligands via invariant TCR and NKG2D, secrete Th1 cytokines (e.g., IFN-γ), activate NK cells, CD8 T cells, and macrophages, and directly lyse tumor cells to remodel the tumor microenvironment.
YES
DIRECT
iNKT cells in AgenT-797 express NKG2D, which binds ULBP1 on target cells and triggers cytotoxic degranulation (perforin/granzyme) leading to direct lysis.