Cell-based cancer vaccine in which a patient's own dendritic cells are loaded with patient-specific neoantigen peptides to present via MHC I/II and prime/expand CD8+ cytotoxic and CD4+ helper T-cell responses.
Autologous dendritic cells are loaded ex vivo with patient-specific neoantigen peptides and reinfused to present these antigens via MHC I/II with costimulatory signals, thereby priming and expanding tumor-specific CD8+ cytotoxic and CD4+ helper T cells to mount durable antitumor immune responses.
NO
INDIRECT
The vaccine primes neoantigen-specific CD8 T cells, which kill tumor cells only if they present the neoantigen peptide in MHC I (e.g., HLA-C) via perforin/granzyme or Fas–FasL; HLA-C itself is not the cytotoxic target.
Cell-based cancer vaccine in which a patient's own dendritic cells are loaded with patient-specific neoantigen peptides to present via MHC I/II and prime/expand CD8+ cytotoxic and CD4+ helper T-cell responses.
Autologous dendritic cells are loaded ex vivo with patient-specific neoantigen peptides and reinfused to present these antigens via MHC I/II with costimulatory signals, thereby priming and expanding tumor-specific CD8+ cytotoxic and CD4+ helper T cells to mount durable antitumor immune responses.
NO
INDIRECT
The DC vaccine presents neoantigen peptides via MHC I/II to prime tumor-specific T cells; cytotoxic CD8 T cells then kill tumor cells displaying the neoantigens on MHC I. HLA-DRB1 (MHC II)–expressing cells are not directly targeted or killed.
Cell-based cancer vaccine in which a patient's own dendritic cells are loaded with patient-specific neoantigen peptides to present via MHC I/II and prime/expand CD8+ cytotoxic and CD4+ helper T-cell responses.
Autologous dendritic cells are loaded ex vivo with patient-specific neoantigen peptides and reinfused to present these antigens via MHC I/II with costimulatory signals, thereby priming and expanding tumor-specific CD8+ cytotoxic and CD4+ helper T cells to mount durable antitumor immune responses.
NO
INDIRECT
The DC vaccine primes neoantigen-specific T cells, which kill tumor cells presenting those neoantigen peptides (mainly via MHC I) by perforin/granzyme or Fas–FasL. HLA-DQA1 expression itself is not a cytotoxic target.
Cell-based cancer vaccine in which a patient's own dendritic cells are loaded with patient-specific neoantigen peptides to present via MHC I/II and prime/expand CD8+ cytotoxic and CD4+ helper T-cell responses.
Autologous dendritic cells are loaded ex vivo with patient-specific neoantigen peptides and reinfused to present these antigens via MHC I/II with costimulatory signals, thereby priming and expanding tumor-specific CD8+ cytotoxic and CD4+ helper T cells to mount durable antitumor immune responses.
NO
INDIRECT
The DC vaccine primes neoantigen-specific T cells, which then kill tumor cells presenting the cognate peptide–MHC complexes (mainly via MHC I) through perforin/granzyme or Fas–FasL pathways. HLA-DQB1 expression itself is not targeted for killing.
An autologous NKG2D-based CAR T-cell therapy in which patient T cells are gene-engineered to express a chimeric antigen receptor using the NKG2D receptor ectodomain fused to intracellular activation/costimulatory domains (e.g., CD3ζ). The cells target stress-induced NKG2D ligands (MICA, MICB, ULBP1–6) on tumor cells to mediate cytotoxicity and cytokine release.
Autologous T cells are engineered to express an NKG2D-based CAR (NKG2D ectodomain fused to 4-1BB and CD3ζ signaling domains) that recognizes stress-induced NKG2D ligands (MICA, MICB, ULBP1–6) on tumors, activating T cells to release cytokines and mediate perforin/granzyme-dependent cytotoxicity against NKG2DL-positive cancer cells.
YES
DIRECT
NKG2D-based CAR T cells recognize ULBP1 on target cells, activate, and induce perforin/granzyme-mediated cytolysis with cytokine release.