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The anti-FR-β antigen-armed antibody (AgAb) is an experimental immunotherapy construct designed for the treatment of acute myeloid leukemia (AML). Developed through research at the German Cancer Research Center (DKFZ) and the University of Heidelberg, this therapeutic consists of a monoclonal antibody targeting folate receptor beta (FR-β)—a surface marker frequently upregulated on AML blasts—fused to immunodominant epitopes from the Epstein-Barr virus (EBV). The mechanism of action involves the antibody binding to FR-β, followed by receptor-mediated endocytosis. Once internalized, the viral epitopes are processed and shuttled to the endosomal compartments for presentation on the cell surface via MHC class II molecules. This strategy effectively 'arms' the tumor cells with viral antigens, redirecting existing endogenous EBV-specific memory CD4+ cytotoxic T cells to recognize and lyse the leukemia cells. This approach aims to bypass the low basal immunogenicity of AML cells by leveraging the potent anti-viral immunity present in the majority of the human population.
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