Autologous chimeric antigen receptor T-cell therapy engineered to recognize BCMA (TNFRSF17) on malignant plasma cells and mediate targeted cytotoxic killing.
Autologous T cells are genetically engineered to express a chimeric antigen receptor specific for BCMA (TNFRSF17) on malignant plasma cells. Upon BCMA binding, CAR signaling (CD3ζ with co-stimulatory domains) activates the T cells, driving proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of BCMA-expressing cells.
CAR T cells recognize BCMA via the CAR, become activated, and kill BCMA-expressing cells through perforin/granzyme-mediated cytolysis (and related 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.
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.
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.
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.
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).