Autologous ex vivo–expanded tumor-infiltrating T cells administered as adoptive cell transfer to mediate antitumor immunity after lymphodepleting conditioning.
Autologous tumor-infiltrating T cells are isolated from the patient’s tumor, expanded ex vivo, and reinfused after lymphodepleting conditioning. These polyclonal T cells use their native TCRs to recognize patient-specific tumor antigens in an HLA-restricted manner, engraft and expand (often supported by IL-2), and mediate antitumor effects via cytotoxic granule release and cytokine secretion.
YES
DIRECT
TILs use native TCRs to recognize the tumor peptide–HLA-DQ complex and directly kill target cells via perforin/granzyme-mediated cytolysis and Fas–FasL apoptosis, with supportive cytokine (e.g., IFN-γ/TNF) effects.
Intratumoral peptide-based immunotherapy designed to present immunogenic CMV/EBV viral peptides to recruit pre-existing virus-specific memory CD8+ T cells, inducing local cytotoxicity, inflammatory cytokines, dendritic cell activation, and epitope spreading to tumor antigens.
Intratumoral administration of immunogenic CMV/EBV-derived peptides (HLA-A*0201–restricted) to present on tumor MHC-I, recruiting and activating pre-existing virus-specific memory CD8+ T cells. This triggers local cytotoxicity and inflammatory cytokines, activates dendritic cells, and drives cross-priming/epitope spreading to tumor antigens; designed to synergize with PD-1/PD-L1 blockade.
YES
INDIRECT
Intratumorally delivered CMV/EBV peptides load onto HLA-A*02:01 on tumor cells; pre-existing virus-specific CD8+ T cells recognize the peptide–HLA complex and kill the presenting cells via perforin/granzyme (and Fas–FasL) cytotoxicity. Killing requires peptide presentation on HLA-A*02:01.
Intratumoral peptide-based immunotherapy designed to present immunogenic CMV/EBV viral peptides to recruit pre-existing virus-specific memory CD8+ T cells, inducing local cytotoxicity, inflammatory cytokines, dendritic cell activation, and epitope spreading to tumor antigens.
Intratumoral administration of immunogenic CMV/EBV-derived peptides (HLA-A*0201–restricted) to present on tumor MHC-I, recruiting and activating pre-existing virus-specific memory CD8+ T cells. This triggers local cytotoxicity and inflammatory cytokines, activates dendritic cells, and drives cross-priming/epitope spreading to tumor antigens; designed to synergize with PD-1/PD-L1 blockade.
YES
DIRECT
Intratumorally delivered CMV pp65 peptide binds MHC-I (HLA-A*02:01) on cells; pre-existing CMV-specific CD8+ T cells recognize peptide–MHC and lyse those cells via perforin/granzyme (and Fas–FasL) cytotoxicity.
Intratumoral peptide-based immunotherapy designed to present immunogenic CMV/EBV viral peptides to recruit pre-existing virus-specific memory CD8+ T cells, inducing local cytotoxicity, inflammatory cytokines, dendritic cell activation, and epitope spreading to tumor antigens.
Intratumoral administration of immunogenic CMV/EBV-derived peptides (HLA-A*0201–restricted) to present on tumor MHC-I, recruiting and activating pre-existing virus-specific memory CD8+ T cells. This triggers local cytotoxicity and inflammatory cytokines, activates dendritic cells, and drives cross-priming/epitope spreading to tumor antigens; designed to synergize with PD-1/PD-L1 blockade.
YES
INDIRECT
Intratumoral EBV peptides are presented on HLA-A*02:01 by tumor cells, recruiting pre-existing EBV-specific CD8+ T cells that recognize peptide–MHC and kill targets via perforin/granzyme (and death receptor) pathways.
Autologous CAR T-cell therapy engineered to express a chimeric antigen receptor targeting guanylyl cyclase C (GCC) on tumor cells, activating T-cell cytotoxicity and cytokine release.
Autologous T cells are genetically engineered (via lentiviral vector) to express a chimeric antigen receptor that binds guanylyl cyclase C (GUCY2C/GCC) on tumor cells. CAR engagement activates T-cell signaling, leading to proliferation, cytokine release, and cytotoxic killing (e.g., perforin/granzyme) of GCC-expressing cancer cells.
YES
DIRECT
CAR T cells bind GCC on target cells, become activated, and kill via perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis) of GCC-expressing cells.