THE ROLE OF COMPLEMENT IN MYELIN PHAGOCYTOSIS DURING PNS WALLERIAN DEGENERATION
THE ROLE OF COMPLEMENT IN MYELIN PHAGOCYTOSIS DURING PNS WALLERIAN DEGENERATION
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DOI：
10.1016/0022-510x(91)90162-z
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发表时间：
1991-06-01
影响因子：
4.4
通讯作者：
FRIEDE, RL
中科院分区：
文献类型：
--
作者：
BRUCK, W;FRIEDE, RL
发生华勒变性的神经中髓磷脂的去除主要取决于入侵的非驻留巨噬细胞。本研究阐明了血清补体成分在体外和体内这一过程中的作用。在 C3 缺乏血清存在的情况下，体外与退化神经共培养的巨噬细胞无法侵入这些神经。细胞侵袭后使用 C3 缺乏血清消除了侵袭巨噬细胞的髓磷脂吞噬能力。这表明补体成分对髓磷脂的调理作用是通过巨噬细胞受体摄取髓磷脂所必需的。在体内，巨噬细胞补体受体 3 型 (CR3) 的单克隆抗体显着降低了髓磷脂的吞噬作用。抗 C3 抗体的免疫组织化学显示退化神经有明显反应。免疫电子显微镜将 C3 颗粒定位在退化的髓鞘处。侵入退化神经的造血细胞也对其细胞质中的C3表现出强烈的反应。这些结果表明，补体成分在巨噬细胞侵袭退化神经和这些细胞摄取髓磷脂方面发挥着关键作用。
Myelin removal in nerves undergoing wallerian degeneration mainly depends on invading, non-resident macrophages. The present study clarifies the role of serum complement components in this process in vitro and in vivo. Macrophages cocultured with degenerating nerves in vitro were unable to invade these nerves in the presence of C3-deficient serum. Application of C3-deficient serum subsequent to cellular invasion abolished the myelin phagocytic capacity of the invaded macrophages. This indicates that opsonization of myelin by complement components is necessary in myelin ingestion via macrophage receptors. In vivo, a monoclonal antibody to the macrophage complement receptor type 3 (CR3) significantly reduced myelin phagocytosis. Immunohistochemistry with anti-C3 antibodies showed a marked reaction in degenerating nerves. Immunoelectron microscopy localized C3 particles at the degenerating myelin sheaths. Haematogenous cells, invading the degenerating nerves, also showed a strong reaction for C3 in their cytoplasm. These results indicate that complement components play a critical role both in macrophage invasion of degenerating nerves and in the ingestion of myelin by these cells.