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首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Complement regulatory proteins and selective vulnerability of neurons to lysis on exposure to acetylcholinesterase antibody.
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Complement regulatory proteins and selective vulnerability of neurons to lysis on exposure to acetylcholinesterase antibody.

机译：补充调节蛋白和神经元对乙酰胆碱酯酶抗体暴露后裂解的选择性脆弱性。

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摘要

Systemic injection of antibodies against acetylcholinesterase (AChE) induces complement-mediated destruction of preganglionic nerve terminals in paravertebral sympathetic ganglia, but spares other AChE-rich structures, such as nerve terminals in prevertebral sympathetic ganglia, parasympathetic ganglia, and the neuromuscular junction. This pattern of differing sensitivity to "AChE immunolesion" might be explained by a differing expression of proteins that serve to protect host cells from complement activation. Two major complement regulatory proteins in rats are Crry, which interferes with the assembly of C3 convertase, and CD59, which blocks formation of the terminal cytolytic membrane attack complex. The present study used immunohistochemistry to demonstrate an inverse relation between levels of CD59 and Crry expression and sensitivity to AChE immunolesion in several AChE-rich targets. Thus, the most sensitive structures, i.e., preganglionic nerve terminals in the adrenal gland and superior cervical ganglion (SCG), expressed undetectable levels of CD59 and Crry immunoreactivities. By contrast, AChE-rich, but antibody-resistant, cholinergic nerve terminals in the inferior mesenteric ganglia (IMG) and diaphragm muscle expressed significant amounts of CD59 and Crry. Such expression was functionally important because, after membrane-anchored CD59 was removed from explanted IMG with phosphatidylinositol phospholipase C, exposure to AChE antibody and complement caused greater immunolesion. It was concluded that differential expression of regulatory proteins in different parts of the nervous system influences regional vulnerability to complement mediated damage.
机译：全身注射针对乙酰胆碱酯酶（AChE）的抗体可诱导补体介导的椎旁交感神经节中神经节前神经末梢的破坏，但保留了其他富含AChE的结构，例如椎前交感神经节，副交感神经节和神经肌肉接头。对“ AChE免疫病变”敏感性不同的这种模式可能是由于蛋白质的不同表达所引起的，这些蛋白质可以保护宿主细胞免于补体激活。大鼠中两个主要的补体调节蛋白是Crry，它干扰C3转化酶的组装;而CD59，它阻止末端细胞溶解膜攻击复合物的形成。本研究使用免疫组织化学证明了在一些富含AChE的靶标中CD59和Crry表达水平与对AChE免疫损害的敏感性之间存在反比关系。因此，最敏感的结构，即肾上腺和上颈神经节（SCG）的神经节前神经末梢，表达出无法检测到的CD59和Crry免疫反应性水平。相比之下，肠系膜下神经节（IMG）和diaphragm肌中富含AChE但具有抗药性的胆碱能神经末梢表达了大量CD59和Crry。这种表达在功能上很重要，因为在用磷脂酰肌醇磷脂酶C将膜锚定的CD59从植入的IMG中去除后，暴露于AChE抗体和补体会引起更大的免疫损伤。结论是，调节蛋白在神经系统不同部位的差异表达影响区域补体介导的损伤的脆弱性。

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