Autologous neoantigen-targeted T cell therapy: ex vivo expanded patient PBMC-derived cytotoxic T cells (primarily CD8+) specific to personalized tumor neoantigens; mediate TCR-dependent recognition of neoantigen–HLA class I on tumor cells and kill via perforin/granzyme.
Autologous PBMC-derived cytotoxic T cells (primarily CD8+) are ex vivo expanded and selected for specificity to patient-specific tumor neoantigens. These unengineered T cells use their endogenous TCRs to recognize neoantigen peptides presented on HLA class I on tumor cells, leading to targeted killing via perforin/granzyme-mediated cytolysis.
YES
DIRECT
Tumor cells presenting the patient-specific neoantigen peptide on HLA-A*02:01 are recognized by the infused neoantigen-specific CD8+ T cells via their endogenous TCRs, leading to perforin/granzyme-mediated cytolysis (with possible Fas–FasL apoptosis).
Autologous neoantigen-targeted T cell therapy: ex vivo expanded patient PBMC-derived cytotoxic T cells (primarily CD8+) specific to personalized tumor neoantigens; mediate TCR-dependent recognition of neoantigen–HLA class I on tumor cells and kill via perforin/granzyme.
Autologous PBMC-derived cytotoxic T cells (primarily CD8+) are ex vivo expanded and selected for specificity to patient-specific tumor neoantigens. These unengineered T cells use their endogenous TCRs to recognize neoantigen peptides presented on HLA class I on tumor cells, leading to targeted killing via perforin/granzyme-mediated cytolysis.
YES
DIRECT
Endogenous TCRs on infused neoantigen-specific CD8+ T cells recognize the patient-specific peptide presented on HLA-A*11:01 and kill target cells via perforin/granzyme-mediated cytolysis (± Fas–FasL apoptosis).
Autologous neoantigen-targeted T cell therapy: ex vivo expanded patient PBMC-derived cytotoxic T cells (primarily CD8+) specific to personalized tumor neoantigens; mediate TCR-dependent recognition of neoantigen–HLA class I on tumor cells and kill via perforin/granzyme.
Autologous PBMC-derived cytotoxic T cells (primarily CD8+) are ex vivo expanded and selected for specificity to patient-specific tumor neoantigens. These unengineered T cells use their endogenous TCRs to recognize neoantigen peptides presented on HLA class I on tumor cells, leading to targeted killing via perforin/granzyme-mediated cytolysis.
YES
DIRECT
Neoantigen-specific CD8+ T cells recognize the HLA-A*24:02–presented neoantigen via their endogenous TCRs and directly kill target cells through perforin/granzyme-mediated cytolysis (± Fas–FasL).
Fc-enhanced anti-CD19 IgG1 monoclonal antibody inducing ADCC/ADCP and apoptosis of malignant CD19+ B cells.
Fc-enhanced humanized anti-CD19 IgG1 monoclonal antibody that binds CD19 on B cells and promotes their elimination via enhanced Fcγ receptor–mediated ADCC and ADCP, with additional direct pro‑apoptotic activity.
YES
DIRECT
Anti-CD19 IgG1 binds CD19 on B cells and engages Fcγ receptor–bearing effector cells to mediate ADCC and ADCP; it can also trigger direct pro‑apoptotic signaling in CD19+ cells.
Autologous tumor-infiltrating lymphocyte (TIL) adoptive cell therapy consisting of ex vivo–expanded, polyclonal CD8+/CD4+ T cells that recognize patient-specific tumor antigens via native TCRs and kill tumor cells through cytotoxic granules and cytokines.
Autologous ex vivo–expanded polyclonal CD8+/CD4+ tumor-infiltrating lymphocytes that recognize patient-specific tumor antigens via native TCRs and eliminate tumor cells through perforin/granzyme-mediated cytotoxicity and cytokine secretion (e.g., IFN-γ, TNF).
YES
DIRECT
Adoptively transferred TILs recognize the neoantigen peptide–HLA class I complex via native TCRs and directly lyse the presenting cell through perforin/granzyme-mediated cytotoxicity (and death-receptor pathways), with cytokines such as IFN-γ/TNF augmenting killing.