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Protective effect of scFv‐DAF fusion protein on the complement attack to acetylcholine receptor: A possible option for treatment of myasthenia gravis

Introduction: Autoantibody‐induced complement activation, which causes disruption of the postsynaptic membrane, is recognized as a key pathogenic factor in myasthenia gravis (MG). Therefore, specific targeting of complement inhibitors to the site of complement activation is a potential therapeutic strategy for treatment of MG. Methods: We assessed expression of single‐chain antibody fragment–decay accelerating factor (scFv‐DAF), comprising a single‐chain fragment scFv1956 based on the rat complement inhibitor DAF in prokaryotic systems, and studied its inhibitory effect on complement deposition in vitro. Results: The recombinant conjugate scFv‐DAF completely retained the wild‐type binding activity of scFv1956 to AChR and inhibited complement activation of DAF in vitro. Conclusions: We found that scFv‐DAF could bind specifically to TE671 cells, and it is significantly more potent at inhibiting complement deposition than the untargeted parent molecule DAF. scFv‐DAF may be a candidate for in vivo protection of the AChR in MG. Muscle Nerve, 2012