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.
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.
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.
An autologous, genetically engineered BCMA-targeted CAR T-cell therapy designed to deplete BCMA-expressing plasmablasts and long-lived plasma cells to reduce pathogenic autoantibodies in refractory lupus nephritis and IgG4-related disease.
Autologous T cells are genetically engineered to express a BCMA-targeted chimeric antigen receptor. After infusion, these CAR T cells recognize and kill BCMA-expressing plasmablasts and long-lived plasma cells, depleting autoantibody-producing cells and reducing pathogenic antibodies in refractory lupus nephritis and IgG4-related disease.
BCMA-targeted CAR T cells bind BCMA on plasmablasts/plasma cells and induce T-cell–mediated killing via perforin/granzyme release and death-receptor pathways.
B7-H4-targeting antibody-drug conjugate delivering a topoisomerase I inhibitor payload to induce DNA damage and tumor cell death.
Humanized IgG1 anti-B7-H4 antibody linked via a protease-cleavable linker to a topoisomerase I inhibitor. After binding B7-H4 on tumor cells and internalization, the payload inhibits TOP1 by stabilizing TOP1-DNA cleavage complexes, blocking DNA re-ligation and causing DNA strand breaks, cell-cycle arrest, and apoptosis in B7-H4-expressing tumor cells.
ADC binds B7-H4 on target cells, is internalized, and releases a topoisomerase I inhibitor that stabilizes TOP1-DNA cleavage complexes, causing DNA breaks, cell-cycle arrest, and apoptosis.