期刊
AMERICAN JOURNAL OF PATHOLOGY
卷 157, 期 3, 页码 905-918出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/S0002-9440(10)64604-4
关键词
-
类别
This study investigated the capacity of neurons and astrocytes to spontaneously activate the complement system and control activation by expressing complement regulators. Human fetal neurons spontaneously activated complement through the classical pathway in normal and immunoglobulin-deficient serum and Clq binding was noted on neurons but not on astrocytes, A strong staining for C4, C3b, iC3b neoepitope and C9 neoepitope was also found on neurons. More than 40% of human fetal neurons were lysed when exposed to normal human serum in the presence of a CD59-blocking antibody, whereas astrocytes were unaffected. Significant reduction in neuronal cell lysis was observed after the addition of soluble complement receptor 1 at 10 mu g/ml. Fetal neurons were stained for CD59 and CD46 and were negative for CD55 and CD35. in contrast, fetal astrocytes were strongly stained for CD59, CD46, CD55, and were negative for CD35, This study demonstrates that human fetal neurons activate spontaneously the classical pathway of complement in an antibody-independent manner to assemble the cytolytic membrane attack complex on their membranes, whereas astrocytes ate unaffected. One reason for the susceptibility of neurons to complement-mediated damage in vivo may reside in their poor capacity to control complement activation.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据