Gene-engineered natural killer (NK) cells expressing a chimeric antigen receptor based on NKG2D to recognize stress-inducible ligands (e.g., MICA, MICB, ULBPs) on AML cells and trigger NK cytotoxicity via DAP10/CD3ζ signaling.
Gene-engineered NK cells expressing an NKG2D-based chimeric antigen receptor recognize stress-inducible ligands (MICA/MICB/ULBPs) on AML cells and signal via DAP10/CD3ζ to activate NK cytotoxicity, leading to perforin/granzyme-mediated killing and cytokine release against leukemic cells.
YES
DIRECT
NKG2D CAR on NK cells binds ULBP2 on target cells, signaling via DAP10/CD3ζ to activate NK degranulation and kill targets through perforin/granzyme-mediated cytolysis (and death receptor pathways).
Gene-engineered natural killer (NK) cells expressing a chimeric antigen receptor based on NKG2D to recognize stress-inducible ligands (e.g., MICA, MICB, ULBPs) on AML cells and trigger NK cytotoxicity via DAP10/CD3ζ signaling.
Gene-engineered NK cells expressing an NKG2D-based chimeric antigen receptor recognize stress-inducible ligands (MICA/MICB/ULBPs) on AML cells and signal via DAP10/CD3ζ to activate NK cytotoxicity, leading to perforin/granzyme-mediated killing and cytokine release against leukemic cells.
YES
DIRECT
NKG2D CAR-NK cells bind ULBP3 on target cells, signal via DAP10/CD3ζ, and kill through NK degranulation (perforin/granzyme-mediated cytolysis; may also engage death receptor pathways).
A personalized cancer vaccine composed of patient-specific tumor neoantigens administered subcutaneously to load antigen-presenting cells (primarily dendritic cells), enhance MHC I/II presentation, and expand tumor-specific CD8+ cytotoxic and CD4+ helper T cells to eliminate residual micrometastatic disease and establish immune memory in post-resection stage IIIA lung adenocarcinoma.
Personalized neoantigen peptide vaccine given subcutaneously to be taken up by antigen‑presenting cells (mainly dendritic cells), enhancing MHC I/II presentation and priming/expanding neoantigen‑specific CD8+ cytotoxic and CD4+ helper T cells to eradicate residual tumor cells and establish durable immune memory.
NO
INDIRECT
The vaccine primes neoantigen-specific T cells via antigen presentation by APCs; the expanded T cells kill cells presenting the specific neoantigen peptides (via MHC I/II) through perforin/granzyme or Fas–FasL. HLA-DP expression itself is not the cytotoxic target.
Gene-engineered natural killer (NK) cells expressing a chimeric antigen receptor based on NKG2D to recognize stress-inducible ligands (e.g., MICA, MICB, ULBPs) on AML cells and trigger NK cytotoxicity via DAP10/CD3ζ signaling.
Gene-engineered NK cells expressing an NKG2D-based chimeric antigen receptor recognize stress-inducible ligands (MICA/MICB/ULBPs) on AML cells and signal via DAP10/CD3ζ to activate NK cytotoxicity, leading to perforin/granzyme-mediated killing and cytokine release against leukemic cells.
YES
DIRECT
NKG2D CAR on NK cells binds ULBP4 on target cells, signaling via DAP10/CD3ζ to activate NK degranulation and kill via perforin/granzyme-mediated apoptosis (with possible FasL/TRAIL contributions).
Gene-engineered natural killer (NK) cells expressing a chimeric antigen receptor based on NKG2D to recognize stress-inducible ligands (e.g., MICA, MICB, ULBPs) on AML cells and trigger NK cytotoxicity via DAP10/CD3ζ signaling.
Gene-engineered NK cells expressing an NKG2D-based chimeric antigen receptor recognize stress-inducible ligands (MICA/MICB/ULBPs) on AML cells and signal via DAP10/CD3ζ to activate NK cytotoxicity, leading to perforin/granzyme-mediated killing and cytokine release against leukemic cells.
YES
DIRECT
NKG2D CAR on NK cells binds ULBP5 on target cells, activating DAP10/CD3ζ signaling and NK effector function, resulting in perforin/granzyme-mediated killing (and death receptor pathways).