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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 >Membrane attack complex of complement is not essential for immune mediated demyelination in experimental autoimmune neuritis.
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Membrane attack complex of complement is not essential for immune mediated demyelination in experimental autoimmune neuritis.

机译：补体的膜攻击复合物对于实验性自身免疫性神经炎的免疫介导的脱髓鞘作用不是必需的。

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Antibody deposition and complement activation, especially membrane attack complex (MAC) formation are considered central for immune mediated demyelination. To examine the role of MAC in immune mediated demyelination, we studied experimental allergic neuritis (EAN) in Lewis rats deficient in complement component 6 (C6) that cannot form MAC. A C6 deficient Lewis (Lewis/C6-) strain of rats was bred by backcrossing the defective C6 gene, from PVG/C6- rats, onto the Lewis background. Lewis/C6- rats had the same C6 gene deletion as PVG/C6- rats and their sera did not support immune mediated haemolysis unless C6 was added. Active EAN was induced in Lewis and Lewis/C6- rats by immunization with bovine peripheral nerve myelin in complete Freund's adjuvant (CFA), and Lewis/C6- rats had delayed clinical EAN compared to the Lewis rats. Peripheral nerve demyelination in Lewis/C6- was also delayed but was similar in extent at the peak of disease. Compared to Lewis, Lewis/C6- nerves had no MAC deposition, reduced macrophage infiltrate and IL-17A, but similar T cell infiltrate and Th1 cytokine mRNA expression. ICAM-1 and P-selectin mRNA expression and immunostaining on vascular endothelium were delayed in Lewis C6- compared to Lewis rats' nerves. This study found that MAC was not required for immune mediated demyelination; but that MAC enhanced early symptoms and early demyelination in EAN, either by direct lysis or by sub-lytic induction of vascular endothelial expression of ICAM-1 and P-selectin.
机译：抗体沉积和补体激活，尤其是膜攻击复合物（MAC）形成被认为是免疫介导的脱髓鞘的关键。为了检查MAC在免疫介导的脱髓鞘中的作用，我们在缺乏补体成分6（C6）且无法形成MAC的Lewis大鼠中研究了实验性过敏性神经炎（EAN）。通过将来自PVG / C6-大鼠的有缺陷的C6基因回交到Lewis背景上来繁殖C6缺陷的Lewis（Lewis / C6-）大鼠品系。 Lewis / C6-大鼠具有与PVG / C6-大鼠相同的C6基因缺失，除非添加C6，否则其血清不支持免疫介导的溶血作用。在完全弗氏佐剂（CFA）中用牛外周神经髓磷脂免疫，在Lewis和Lewis / C6-大鼠中诱导了活动性EAN，与Lewis大鼠相比，Lewis / C6-大鼠的临床EAN延迟。 Lewis / C6-的周围神经脱髓鞘也被延迟，但在疾病高峰期的程度相似。与Lewis相比，Lewis / C6-神经没有MAC沉积，巨噬细胞浸润和IL-17A减少，但T细胞浸润和Th1细胞因子mRNA表达相似。与Lewis大鼠的神经相比，Lewis C6-中ICAM-1和P-selectin mRNA的表达以及在血管内皮上的免疫染色被延迟。这项研究发现，免疫介导的脱髓鞘作用不需要MAC。但是MAC通过直接裂解或亚裂解诱导ICAM-1和P-选择素的血管内皮表达增强了EAN中的早期症状和早期脱髓鞘。

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