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本文引用的文献

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An improved method for refolding recombinant decay accelerating factor for therapeutic studies.一种用于治疗研究的重组衰变加速因子复性的改进方法。
Protein Expr Purif. 2009 Jul;66(1):102-6. doi: 10.1016/j.pep.2009.02.014. Epub 2009 Feb 28.
2
Anti-C5 antibody treatment ameliorates weakness in experimentally acquired myasthenia gravis.抗C5抗体治疗可改善实验性获得性重症肌无力的肌无力症状。
J Immunol. 2007 Dec 15;179(12):8562-7. doi: 10.4049/jimmunol.179.12.8562.
3
Gene splicing and mutagenesis by PCR-driven overlap extension.通过PCR驱动的重叠延伸进行基因剪接和诱变。
Nat Protoc. 2007;2(4):924-32. doi: 10.1038/nprot.2007.132.
4
The membrane attack pathway of complement drives pathology in passively induced experimental autoimmune myasthenia gravis in mice.补体的膜攻击途径在被动诱导的小鼠实验性自身免疫性重症肌无力中引发病理变化。
Clin Exp Immunol. 2006 Nov;146(2):294-302. doi: 10.1111/j.1365-2249.2006.03205.x.
5
Complement membrane attack is required for endplate damage and clinical disease in passive experimental myasthenia gravis in Lewis rats.在Lewis大鼠被动实验性重症肌无力中，补体膜攻击对于终板损伤和临床疾病是必需的。
Clin Exp Immunol. 2006 Nov;146(2):278-86. doi: 10.1111/j.1365-2249.2006.03198.x.
6
Autoimmune channelopathies and related neurological disorders.自身免疫性离子通道病及相关神经系统疾病。
Neuron. 2006 Oct 5;52(1):123-38. doi: 10.1016/j.neuron.2006.09.024.
7
Deficiency of decay accelerating factor and CD59 leads to crisis in experimental myasthenia.衰变加速因子和CD59的缺乏会导致实验性重症肌无力危象。
Exp Neurol. 2006 Dec;202(2):287-93. doi: 10.1016/j.expneurol.2006.06.003. Epub 2006 Jul 20.
8
ScFv-mediated in vivo targeting of DAF to erythrocytes inhibits lysis by complement.单链抗体片段介导的衰变加速因子在体内靶向红细胞可抑制补体介导的细胞溶解。
Mol Immunol. 2004 Feb;40(13):911-9. doi: 10.1016/j.molimm.2003.10.017.
9
Complement receptor 2-mediated targeting of complement inhibitors to sites of complement activation.补体受体2介导的补体抑制剂靶向作用于补体激活部位。
J Clin Invest. 2003 Jun;111(12):1875-85. doi: 10.1172/JCI17348.
10
Markedly enhanced susceptibility to experimental autoimmune myasthenia gravis in the absence of decay-accelerating factor protection.在缺乏衰变加速因子保护的情况下，对实验性自身免疫性重症肌无力的易感性显著增强。
J Clin Invest. 2002 Nov;110(9):1269-74. doi: 10.1172/JCI16086.

scFv-DAF 融合蛋白对乙酰胆碱受体补体攻击的保护作用：治疗重症肌无力的一种可能选择。

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

机构信息

Department of Neurology, Tangdu Hospital, Fourth Military Medical University, Xi'an, China.

Department of Microbiology, Fourth Military Medical University, Xi'an, China.

出版信息

Muscle Nerve. 2012 May;45(5):668-675. doi: 10.1002/mus.23247.

DOI:10.1002/mus.23247
PMID:22499093
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4308948/
Abstract

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.

摘要

简介

自身抗体诱导的补体激活会破坏突触后膜，这被认为是重症肌无力 (MG) 的一个关键致病因素。因此，将补体抑制剂特异性靶向补体激活部位是治疗 MG 的一种潜在治疗策略。

方法

我们评估了单链抗体片段衰变加速因子 (scFv-DAF) 的表达，该片段由基于大鼠补体抑制剂 DAF 的原核系统中的单链片段 scFv1956 组成，并研究了其在体外对补体沉积的抑制作用。

结果

重组缀合物 scFv-DAF 完全保留了 scFv1956 对 AChR 的野生型结合活性，并在体外抑制了 DAF 的补体激活。

结论

我们发现 scFv-DAF 可以特异性结合 TE671 细胞，并且在抑制补体沉积方面比非靶向亲本分子 DAF 更有效。scFv-DAF 可能是体内保护 MG 中 AChR 的候选物。