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B-cell maturation antigen (BCMA) and Cluster of differentiation 3 (CD3) represent a dual-target complex primarily utilized for T-cell redirection therapy in hematological malignancies. BCMA, also known as TNFRSF17, is a cell surface receptor highly expressed on malignant plasma cells in multiple myeloma, where it promotes cell survival and proliferation. CD3 is a multi-subunit protein complex that serves as a co-receptor for the T-cell receptor, playing a critical role in signal transduction and T-cell activation. Bispecific antibodies and T-cell engagers (BiTEs) are designed to bridge these two components, bringing cytotoxic T cells into close proximity with BCMA-expressing tumor cells. This interaction triggers the formation of a cytolytic synapse, leading to the directed release of perforin and granzymes that induce tumor cell apoptosis. While these therapies have shown significant efficacy in relapsed or refractory multiple myeloma, they are associated with notable safety risks such as cytokine release syndrome (CRS) and immune effector cell-associated neurotoxicity syndrome (ICANS). Additionally, the depletion of normal plasma cells can lead to hypogammaglobulinemia and an increased susceptibility to infections.
T-cell redirection, T-cell mediated cytotoxicity, Immune synapse formation, Perforin and granzyme release
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