Autologous ex vivo-expanded T cells isolated from the patient’s tumor, infused to provide tumor-specific cytotoxic CD8+/CD4+ T cells for adoptive cellular immunotherapy.
Autologous tumor-resident T cells isolated from the patient’s tumor are expanded ex vivo and reinfused to provide polyclonal, tumor‑antigen–specific CD8+/CD4+ T cells. These cells recognize tumor antigens via their native TCRs in an MHC-restricted manner and mediate cytotoxicity (perforin/granzyme) and cytokine release to eliminate tumor cells; they are not genetically engineered.
YES
DIRECT
TILs recognize the patient-specific neoantigen peptide–HLA class I complex via native TCRs and directly induce apoptosis via perforin/granzyme (and Fas–FasL) cytotoxic pathways.
Autologous ex vivo-expanded T cells isolated from the patient’s tumor, infused to provide tumor-specific cytotoxic CD8+/CD4+ T cells for adoptive cellular immunotherapy.
Autologous tumor-resident T cells isolated from the patient’s tumor are expanded ex vivo and reinfused to provide polyclonal, tumor‑antigen–specific CD8+/CD4+ T cells. These cells recognize tumor antigens via their native TCRs in an MHC-restricted manner and mediate cytotoxicity (perforin/granzyme) and cytokine release to eliminate tumor cells; they are not genetically engineered.
YES
DIRECT
Autologous TILs recognize the patient-specific tumor peptide–HLA class I complex via native TCRs and kill the presenting cell by perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis).
Autologous cellular immunotherapy using ex vivo–generated dendritic cells pulsed with patient-specific tumor neoantigen peptides to prime/expand neoantigen-specific CD8+ and CD4+ T cells.
Autologous dendritic cells are generated ex vivo and pulsed with patient-specific tumor neoantigen peptides. After infusion, the DCs migrate to lymphoid tissues and present these neoantigens on HLA class I and II, providing costimulation (e.g., CD80/CD86) and cytokines to prime and expand neoantigen-specific CD8+ cytotoxic T cells and CD4+ helper T cells, thereby promoting tumor-specific immune responses and immunologic memory.
NO
INDIRECT
The DC vaccine uses HLA class II on dendritic cells to prime neoantigen-specific T cells; it does not target or kill HLA II+ DCs. Activated CD8+ T cells then kill tumor cells presenting neoantigen on HLA I via perforin/granzyme (and Fas–FasL) pathways.
Autologous ex vivo-expanded T cells isolated from the patient’s tumor, infused to provide tumor-specific cytotoxic CD8+/CD4+ T cells for adoptive cellular immunotherapy.
Autologous tumor-resident T cells isolated from the patient’s tumor are expanded ex vivo and reinfused to provide polyclonal, tumor‑antigen–specific CD8+/CD4+ T cells. These cells recognize tumor antigens via their native TCRs in an MHC-restricted manner and mediate cytotoxicity (perforin/granzyme) and cytokine release to eliminate tumor cells; they are not genetically engineered.
YES
DIRECT
TILs recognize the patient-specific neoantigen peptide presented on HLA class II via their native TCRs and directly kill the presenting tumor cell through perforin/granzyme release and/or Fas–FasL–mediated apoptosis.
Autologous ex vivo-expanded T cells isolated from the patient’s tumor, infused to provide tumor-specific cytotoxic CD8+/CD4+ T cells for adoptive cellular immunotherapy.
Autologous tumor-resident T cells isolated from the patient’s tumor are expanded ex vivo and reinfused to provide polyclonal, tumor‑antigen–specific CD8+/CD4+ T cells. These cells recognize tumor antigens via their native TCRs in an MHC-restricted manner and mediate cytotoxicity (perforin/granzyme) and cytokine release to eliminate tumor cells; they are not genetically engineered.
YES
DIRECT
TILs use native TCRs to recognize the tumor-associated peptide on HLA class II and directly kill antigen-bearing cells via perforin/granzyme release and Fas–FasL–mediated apoptosis.