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 is taken up by HLA‑DR+ antigen‑presenting cells to present neoantigens and expand neoantigen‑specific CD8+ T cells, which kill tumor cells via perforin/granzyme after MHC I recognition; HLA‑DR itself is not a cytotoxic target.
Autologous ex vivo dendritic cell-sensitized cytotoxic T lymphocytes with NK-like cytotoxic features, administered intraperitoneally to kill residual peritoneal tumor cells.
Autologous cytotoxic T lymphocytes expanded ex vivo by dendritic cell sensitization to enrich native TCR tumor specificity; upon intraperitoneal infusion, they kill residual peritoneal tumor cells via antigen-specific TCR recognition and perforin/granzyme release, augmented by NK-like cytotoxic pathways (e.g., NKG2D-mediated killing).
YES
DIRECT
nCTLs express NKG2D that recognizes MICA on target cells, activating cytotoxic granule release (perforin/granzyme) and causing direct lysis/apoptosis.
Autologous ex vivo dendritic cell-sensitized cytotoxic T lymphocytes with NK-like cytotoxic features, administered intraperitoneally to kill residual peritoneal tumor cells.
Autologous cytotoxic T lymphocytes expanded ex vivo by dendritic cell sensitization to enrich native TCR tumor specificity; upon intraperitoneal infusion, they kill residual peritoneal tumor cells via antigen-specific TCR recognition and perforin/granzyme release, augmented by NK-like cytotoxic pathways (e.g., NKG2D-mediated killing).
YES
DIRECT
nCTLs express NKG2D that recognizes MICB on target cells, activating NK-like cytotoxicity and causing direct lysis via perforin/granzyme release.
Autologous ex vivo dendritic cell-sensitized cytotoxic T lymphocytes with NK-like cytotoxic features, administered intraperitoneally to kill residual peritoneal tumor cells.
Autologous cytotoxic T lymphocytes expanded ex vivo by dendritic cell sensitization to enrich native TCR tumor specificity; upon intraperitoneal infusion, they kill residual peritoneal tumor cells via antigen-specific TCR recognition and perforin/granzyme release, augmented by NK-like cytotoxic pathways (e.g., NKG2D-mediated killing).
YES
DIRECT
nCTLs express NKG2D; recognition of ULBP1 on target cells activates cytotoxic granule release (perforin/granzyme) leading to apoptosis/lysis of ULBP1+ cells.
Autologous ex vivo dendritic cell-sensitized cytotoxic T lymphocytes with NK-like cytotoxic features, administered intraperitoneally to kill residual peritoneal tumor cells.
Autologous cytotoxic T lymphocytes expanded ex vivo by dendritic cell sensitization to enrich native TCR tumor specificity; upon intraperitoneal infusion, they kill residual peritoneal tumor cells via antigen-specific TCR recognition and perforin/granzyme release, augmented by NK-like cytotoxic pathways (e.g., NKG2D-mediated killing).
YES
DIRECT
nCTLs express NKG2D; engagement of ULBP2 on target cells activates cytotoxic degranulation (perforin/granzyme) leading to target cell death.