Autologous tumor-infiltrating lymphocyte (TIL) therapy in which a patient’s tumor-resident T cells are expanded ex vivo and reinfused to mediate TCR-dependent cytotoxicity and cytokine release against tumor/HPV antigens, aiming to overcome tumor microenvironment immunosuppression.
Autologous tumor-infiltrating lymphocytes expanded ex vivo are reinfused to recognize tumor/HPV antigens via native TCRs and mediate antitumor effects through cytotoxic killing (perforin/granzyme) and cytokine release (e.g., IFN-γ), aiming to overcome tumor microenvironment immunosuppression.
YES
DIRECT
Infused TILs recognize HPV E6/E7 peptides via native TCRs on antigen-presenting tumor cells and induce apoptosis via perforin/granzyme cytolysis (and Fas–FasL), supported by cytokines such as IFN-γ.
Oral small-molecule BCL-2 inhibitor that blocks anti-apoptotic BCL-2 to trigger mitochondrial apoptosis in AML blasts; given in 28-day cycles post-allogeneic HCT and may continue as monotherapy.
Selective oral BCL-2 inhibitor (BH3 mimetic) that binds the BH3-binding groove of anti-apoptotic BCL-2, neutralizing its pro-survival function and freeing pro-apoptotic effectors to trigger mitochondrial outer membrane permeabilization and caspase-dependent apoptosis in BCL-2–dependent AML cells; spares BCL-XL relative to navitoclax, reducing thrombocytopenia.
YES
DIRECT
Venetoclax binds and inhibits anti-apoptotic BCL-2, freeing pro-apoptotic effectors (e.g., BAX/BAK) to induce mitochondrial outer membrane permeabilization, caspase activation, and intrinsic apoptosis in BCL-2–dependent cells.
Donor-derived antigen-specific CD4+ and CD8+ T lymphocytes selected by IFN-γ capture after brief stimulation with CMV, EBV, and adenovirus peptides; infused as adoptive cellular therapy to restore antiviral immunity in allo-HSCT recipients.
Donor-derived CD4+ and CD8+ T lymphocytes are briefly stimulated with CMV, EBV, and adenovirus peptides and IFN-γ–secreting cells are magnetically captured, enriching for virus-specific TCR specificities. After infusion, these unengineered T cells recognize HLA-presented viral epitopes via their native TCRs, secrete Th1 cytokines (e.g., IFN-γ), and kill infected cells through perforin/granzyme-mediated cytotoxicity, expanding in vivo to restore antiviral immunity in allo-HSCT recipients.
YES
DIRECT
Virus-specific T cells recognize CMV peptide–HLA complexes via their native TCR and induce apoptosis of infected cells through perforin/granzyme-mediated cytotoxicity (± Fas–FasL).
Anti-GD2 IgG1 monoclonal antibody immunotherapy that binds GD2 on neuroblastoma cells and mediates Fc-dependent ADCC, ADCP, and CDC.
Anti-GD2 IgG1 monoclonal antibody that binds GD2 on neuroblastoma cells and triggers Fc-mediated effector functions—ADCC by NK cells, ADCP by macrophages—and complement-dependent cytotoxicity (CDC), leading to tumor cell lysis.
YES
DIRECT
Anti-GD2 IgG1 binds GD2 and recruits immune effectors to kill target cells via Fc-mediated ADCC (NK cells), ADCP (macrophages), and complement-dependent cytotoxicity (CDC) leading to lysis.