Protective effect of scFv-DAF fusion protein on the complement attack to acetylcholine receptor: a possible option for treatment of myasthenia gravis.
Protective effect of scFv-DAF fusion protein on the complement attack to acetylcholine receptor: a possible option for treatment of myasthenia gravis.
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DOI：
10.1002/mus.23247
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发表时间：
2012-05
期刊：
影响因子：
3.4
通讯作者：
Kaminski, Henry J.
中科院分区：
文献类型：
--
作者：
Song, Chen;Xu, Zhikai;Miao, Jianting;Xu, Jiang;Wu, Xingan;Zhang, Fanglin;Lin, Hong;Li, Zhuyi;Kaminski, Henry J.
关键词：
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. 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. The recombinant conjugate scFv-DAF completely retained the wild-type binding activity of scFv1956 to AChR and inhibited complement activation of DAF in vitro. 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.
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