Therapeutic long-peptide cancer vaccine presenting the H3K27M mutant histone H3 neoepitope to prime and expand tumor-specific CD4/CD8 T cells.
Long-peptide vaccine containing the H3K27M neoepitope; after subcutaneous administration it is processed and presented by antigen-presenting cells on MHC I/II to prime and expand H3K27M-specific CD8+ and CD4+ T cells, eliciting cytotoxic T-lymphocyte responses that target and kill H3K27M-expressing tumor cells.
YES
INDIRECT
The peptide vaccine primes and expands H3K27M-specific T cells via APC presentation; CD8+ CTLs recognize H3K27M peptide–MHC I on tumor cells and kill them via perforin/granzyme (and Fas–FasL) pathways.
Therapeutic long-peptide cancer vaccine presenting the H3K27M mutant histone H3 neoepitope to prime and expand tumor-specific CD4/CD8 T cells.
Long-peptide vaccine containing the H3K27M neoepitope; after subcutaneous administration it is processed and presented by antigen-presenting cells on MHC I/II to prime and expand H3K27M-specific CD8+ and CD4+ T cells, eliciting cytotoxic T-lymphocyte responses that target and kill H3K27M-expressing tumor cells.
YES
INDIRECT
The vaccine primes H3K27M-specific CD8+ T cells that recognize H3K27M peptides on MHC I of tumor cells and kill them via CTL mechanisms (perforin/granzyme, Fas–FasL).
Therapeutic long-peptide cancer vaccine presenting the H3K27M mutant histone H3 neoepitope to prime and expand tumor-specific CD4/CD8 T cells.
Long-peptide vaccine containing the H3K27M neoepitope; after subcutaneous administration it is processed and presented by antigen-presenting cells on MHC I/II to prime and expand H3K27M-specific CD8+ and CD4+ T cells, eliciting cytotoxic T-lymphocyte responses that target and kill H3K27M-expressing tumor cells.
YES
INDIRECT
The vaccine primes and expands H3K27M-specific CD8+ T cells; these CTLs recognize H3K27M peptides presented on MHC I of tumor cells and kill them via perforin/granzyme (and Fas–FasL) pathways.
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-CAR T cells bind ULBP4 on target cells, become activated, and kill the engaged cells via perforin/granzyme-mediated cytotoxicity (with associated cytokine release).
An engineered bispecific IgM T-cell–engaging antibody administered intravenously that binds CD38 on myeloma cells and CD3 on T cells, redirecting T cells to mediate T-cell–dependent cellular cytotoxicity and triggering complement-dependent cytotoxicity.
Engineered bispecific IgM antibody that binds CD38 on tumor cells and CD3 on T cells, crosslinking to redirect T cells for T-cell-dependent cellular cytotoxicity; the IgM format also activates complement to mediate complement-dependent cytotoxicity against CD38-positive cells.
YES
DIRECT
Bispecific IgM binds CD38 on target cells and CD3 on T cells to redirect T-cell cytotoxicity, and its IgM format activates complement to mediate complement-dependent lysis of CD38+ cells.