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Development of antagonists that target FcRn, so as to increase IgG catabolism, thus represents a universal, yet targeted approach for the treatment of IgG-mediated autoimmune diseases [22]

BMC Cardiovasc Disord 18(1):23

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Additionally, terminal complement pathway activation generates membrane attack complexes (MAC), which build pores in the MM cell membrane, resulting in direct cell lysis [61, 62]