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Anti-BCMA CAR-T therapy is a form of autologous or allogeneic chimeric antigen receptor T-cell therapy in which T lymphocytes are genetically engineered to express a synthetic receptor targeting B-cell maturation antigen (BCMA), a TNF receptor superfamily protein highly and selectively expressed on malignant plasma cells in multiple myeloma and late-stage B cells. After leukapheresis and ex vivo genetic modification (typically using viral vectors) to introduce a CAR comprising an anti-BCMA single-chain variable fragment, a transmembrane domain, CD3ζ signaling module, and one or more costimulatory domains (commonly 4-1BB or CD28), the expanded cells are reinfused to recognize and bind BCMA on tumor cells, triggering T-cell activation, proliferation, cytokine secretion, and cytolytic killing via perforin–granzyme and death receptor pathways.[1][3][4][5] This therapy has shown high response rates and deep remissions in relapsed or refractory multiple myeloma, but is associated with characteristic toxicities including cytokine release syndrome and neurotoxicity, and resistance mechanisms such as BCMA downregulation, antigen loss, and T-cell exhaustion are active areas of translational optimization.[1][3][7][8][9][10]
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