Allogeneic, cord blood–derived NK cell therapy engineered to express an HLA-A*02:01–restricted NY-ESO-1–specific T-cell receptor plus IL-15 to enhance activation, proliferation, and persistence; mediates tumor killing via the introduced TCR and native NK cytotoxicity.
Allogeneic cord blood–derived NK cells engineered to express an HLA-A*02:01–restricted NY-ESO-1–specific TCR plus IL-15. The introduced TCR enables recognition of NY-ESO-1 peptide–HLA complexes on tumor cells, while IL-15 enhances activation, proliferation, and persistence. Tumor killing occurs via TCR-driven cytotoxicity and native NK effector functions (perforin/granzyme, activating receptors such as NKG2D).
YES
DIRECT
Engineered NK cells bearing an HLA-A*02:01–restricted NY-ESO-1–specific TCR recognize the NY-ESO-1 peptide–HLA complex on target cells and directly induce cytolysis via TCR-triggered perforin/granzyme (and death-receptor) pathways, with IL-15 enhancing activity and persistence.
Allogeneic, cord blood–derived NK cell therapy engineered to express an HLA-A*02:01–restricted NY-ESO-1–specific T-cell receptor plus IL-15 to enhance activation, proliferation, and persistence; mediates tumor killing via the introduced TCR and native NK cytotoxicity.
Allogeneic cord blood–derived NK cells engineered to express an HLA-A*02:01–restricted NY-ESO-1–specific TCR plus IL-15. The introduced TCR enables recognition of NY-ESO-1 peptide–HLA complexes on tumor cells, while IL-15 enhances activation, proliferation, and persistence. Tumor killing occurs via TCR-driven cytotoxicity and native NK effector functions (perforin/granzyme, activating receptors such as NKG2D).
YES
DIRECT
Engineered NK cells expressing an HLA-A*02:01–restricted NY-ESO-1–specific TCR bind the NY-ESO-1 peptide–HLA-A*02:01 complex on target cells and induce cytolysis via perforin/granzyme release (with IL-15 enhancing activity).
Allogeneic, cord blood–derived NK cell therapy engineered to express an HLA-A*02:01–restricted NY-ESO-1–specific T-cell receptor plus IL-15 to enhance activation, proliferation, and persistence; mediates tumor killing via the introduced TCR and native NK cytotoxicity.
Allogeneic cord blood–derived NK cells engineered to express an HLA-A*02:01–restricted NY-ESO-1–specific TCR plus IL-15. The introduced TCR enables recognition of NY-ESO-1 peptide–HLA complexes on tumor cells, while IL-15 enhances activation, proliferation, and persistence. Tumor killing occurs via TCR-driven cytotoxicity and native NK effector functions (perforin/granzyme, activating receptors such as NKG2D).
NO
INDIRECT
Cytotoxicity is mediated by the engineered TCR recognizing NY-ESO-1 peptide–HLA-A*02:01 and by native NK effector pathways (perforin/granzyme). IL-15 enhances NK function. IL-15Rα-expressing cells are not specifically targeted or killed due to IL-15Rα expression.
Allogeneic, cord blood–derived NK cell therapy engineered to express an HLA-A*02:01–restricted NY-ESO-1–specific T-cell receptor plus IL-15 to enhance activation, proliferation, and persistence; mediates tumor killing via the introduced TCR and native NK cytotoxicity.
Allogeneic cord blood–derived NK cells engineered to express an HLA-A*02:01–restricted NY-ESO-1–specific TCR plus IL-15. The introduced TCR enables recognition of NY-ESO-1 peptide–HLA complexes on tumor cells, while IL-15 enhances activation, proliferation, and persistence. Tumor killing occurs via TCR-driven cytotoxicity and native NK effector functions (perforin/granzyme, activating receptors such as NKG2D).
NO
INDIRECT
CD122 (IL-2/IL-15Rβ) is not targeted for killing. The engineered NK cells kill NY-ESO-1 peptide–HLA-A*02:01–positive tumor cells via the introduced TCR (and native NK cytotoxicity). IL-15 signals through CD122 to support NK survival/activation, not to kill CD122-expressing cells.
Allogeneic, cord blood–derived NK cell therapy engineered to express an HLA-A*02:01–restricted NY-ESO-1–specific T-cell receptor plus IL-15 to enhance activation, proliferation, and persistence; mediates tumor killing via the introduced TCR and native NK cytotoxicity.
Allogeneic cord blood–derived NK cells engineered to express an HLA-A*02:01–restricted NY-ESO-1–specific TCR plus IL-15. The introduced TCR enables recognition of NY-ESO-1 peptide–HLA complexes on tumor cells, while IL-15 enhances activation, proliferation, and persistence. Tumor killing occurs via TCR-driven cytotoxicity and native NK effector functions (perforin/granzyme, activating receptors such as NKG2D).
NO
INDIRECT
Engineered NK cells kill NY-ESO-1 peptide–HLA-A*02:01–positive tumor cells via TCR-mediated recognition and perforin/granzyme release. IL-15 signals through CD132 on the NK cells to enhance their function; cells expressing CD132 are not targeted for killing.