Autologous CD8+/CD4+ T cells expanded ex vivo from the patient's tumor to recognize tumor antigens via native TCRs; administered as adoptive cell therapy.
Autologous tumor-infiltrating CD8+/CD4+ T cells expanded ex vivo are reinfused to restore large numbers of tumor-reactive lymphocytes. Using native TCRs, they recognize patient-specific tumor antigens presented on MHC, traffic to tumor sites, and mediate cytotoxicity via perforin/granzyme release and cytokine secretion. Lymphodepletion and IL-2 support enhance in vivo expansion and persistence.
YES
DIRECT
Infused CD8+ TILs recognize the tumor-derived peptide presented by HLA-A via their native TCR and kill target cells by perforin/granzyme-mediated cytolysis and Fas–FasL–induced apoptosis.
Autologous CD8+/CD4+ T cells expanded ex vivo from the patient's tumor to recognize tumor antigens via native TCRs; administered as adoptive cell therapy.
Autologous tumor-infiltrating CD8+/CD4+ T cells expanded ex vivo are reinfused to restore large numbers of tumor-reactive lymphocytes. Using native TCRs, they recognize patient-specific tumor antigens presented on MHC, traffic to tumor sites, and mediate cytotoxicity via perforin/granzyme release and cytokine secretion. Lymphodepletion and IL-2 support enhance in vivo expansion and persistence.
YES
DIRECT
Infused TILs recognize tumor-derived peptides presented by HLA-B class I via their native TCRs and directly kill target cells through perforin/granzyme-mediated cytolysis and Fas–FasL apoptosis, with supportive cytokine effects.
Anti-HER2 humanized monoclonal antibody (Herceptin) that blocks HER2 signaling and mediates ADCC; used for HER2-positive tumors.
Humanized monoclonal antibody against HER2 (ERBB2) that binds the extracellular domain (subdomain IV), blocks HER2 signaling and receptor dimerization, inhibits downstream PI3K–AKT/MAPK pathways, and engages Fcγ receptors to mediate antibody-dependent cellular cytotoxicity (ADCC) in HER2-overexpressing tumors.
YES
DIRECT
Trastuzumab binds HER2 on tumor cells and its Fc engages FcγR+ effector cells (e.g., NK cells) to mediate antibody‑dependent cellular cytotoxicity; it can also activate complement and block HER2 signaling, promoting apoptosis.
Autologous CD8+/CD4+ T cells expanded ex vivo from the patient's tumor to recognize tumor antigens via native TCRs; administered as adoptive cell therapy.
Autologous tumor-infiltrating CD8+/CD4+ T cells expanded ex vivo are reinfused to restore large numbers of tumor-reactive lymphocytes. Using native TCRs, they recognize patient-specific tumor antigens presented on MHC, traffic to tumor sites, and mediate cytotoxicity via perforin/granzyme release and cytokine secretion. Lymphodepletion and IL-2 support enhance in vivo expansion and persistence.
YES
DIRECT
TILs recognize the tumor-derived peptide presented by HLA-C via their native TCRs and directly kill target cells through perforin/granzyme-mediated cytolysis (and death receptor pathways).
Autologous CD8+/CD4+ T cells expanded ex vivo from the patient's tumor to recognize tumor antigens via native TCRs; administered as adoptive cell therapy.
Autologous tumor-infiltrating CD8+/CD4+ T cells expanded ex vivo are reinfused to restore large numbers of tumor-reactive lymphocytes. Using native TCRs, they recognize patient-specific tumor antigens presented on MHC, traffic to tumor sites, and mediate cytotoxicity via perforin/granzyme release and cytokine secretion. Lymphodepletion and IL-2 support enhance in vivo expansion and persistence.
YES
DIRECT
CD4+ TILs recognize tumor-derived peptide–HLA-DR via their native TCRs and directly kill the presenting cell through perforin/granzyme release and Fas–FasL apoptosis, with IFN-γ/TNF-α aiding cytotoxicity.