The role of complement in immunological demyelination of the mammalian spinal cord
The role of complement in immunological demyelination of the mammalian spinal cord
复制标题
DOI：
10.1038/sj.sc.3101737
复制
发表时间：
2005-07-01
期刊：
影响因子：
2.2
通讯作者：
Steeves, JD
中科院分区：
文献类型：
--
作者：
Dyer, JK;Bourque, JA;Steeves, JD
研究设计：血清补体成分诱发免疫性脱髓鞘的特异性。目的：探讨补体成分及其通路在成年大鼠脊髓实验性免疫性脱髓鞘中的作用。单位：加拿大温哥华英属哥伦比亚大学ICORD。实验对象：选用32只成年雄性Sprague-Dawley大鼠，体重约220 g。方法：采用微型渗透泵灌注脱髓鞘药，以0.5 μ l/h滴注，连续7 d。试剂包括半乳糖脑苷多克隆抗体和人血清补体。补体血清缺乏单一组分被用来评估替代途径，经典途径和膜攻击复合物的作用。7天时进行超微结构脱髓鞘评估。结果：去除经典和替代补体途径中常见的C3蛋白，或经典途径蛋白C4蛋白，均未导致脱髓鞘。然而，补体缺乏因子B（一种替代途径蛋白）可产生有效的脱髓鞘。去除C5或C6膜攻击复合蛋白后，还观察到脱髓鞘。结论：这表明经典途径足以使成年大鼠脊髓脱髓鞘，膜攻击复合物也不需要。
Study design: Specificity of serum complement component to elicit immunological demyelination.Objectives: To assess the role of complement components and pathways in experimental immunological demyelination of the adult rat spinal cord.Setting: ICORD, University of British Columbia, Vancouver, Canada.Subjects: We used 32 adult male Sprague-Dawley rats, of approximately 220 g weight.Methods: Rats received intraspinal infusions of demyelinating reagents, delivered by osmotic minipump, for a 7-day infusion at 0.5 mu l/h. Reagents consisted of a polyclonal antibody to galactocerebroside and human serum complement. Complement sera deficient for a single component were used to assess the role of the alternative pathway, the classical pathway, and the membrane attack complex. Demyelination was assessed, at 7 days, ultrastructurally.Results: Removal of C3 protein, common to classical and alternative complement pathways, or C4 protein, a classical pathway protein, resulted in no demyelination. However, complement deficient in Factor B, an alternative pathway protein, produced effective demyelination. Upon removal of C5 or C6, membrane attack complex proteins, demyelination was also observed.Conclusion: This suggests that the classical pathway is sufficient for the protocol to demyelinate the adult rat spinal cord, and that the membrane attack complex is also not required.