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.
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.
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.
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).
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.
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).
Autologous TILs recognize the tumor-associated peptide–HLA class I via native TCRs and directly kill the presenting cells through perforin/granzyme release (and Fas–FasL), with IFN-γ/TNF contributing to apoptosis.