COMPLEMENT RECEPTORS AND REGULATORY PROTEINS IN HUMAN ATHEROSCLEROTIC LESIONS
COMPLEMENT RECEPTORS AND REGULATORY PROTEINS IN HUMAN ATHEROSCLEROTIC LESIONS
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DOI：
10.1161/01.atv.9.6.802
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发表时间：
1989-11-01
期刊：
影响因子：
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通讯作者：
HANSSON, GK
中科院分区：
文献类型：
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作者：
SEIFERT, PS;HANSSON, GK
C5b-9 末端复合物的存在表明人类动脉粥样硬化病变中的补体激活。通过使用补体C3b受体（CR1）和iC3b受体（CR3）的单克隆抗体，观察到复杂的人类颈动脉病变中大约20%的细胞表达CR1和CR3抗原。百分之一到百分之五的补体受体阳性细胞被平滑肌细胞特异性肌球蛋白染色，其余的根据其与抗 LeuM3 (CD14) 单克隆抗体的反应性被确定主要是巨噬细胞。在检查的八个病变中均未观察到 C3dg 受体 (CR2) 阳性细胞。补体调节糖蛋白衰变加速因子 (DAF) 广泛分布于细胞外，占总细胞群的 20% 至 60%。 H 因子是一种调节旁路途径 C3 转化酶形成的血浆蛋白，在 70% 的检查病变中在细胞外观察到了 H 因子。 C1 抑制剂存在于少数斑块样本中，相对稀疏，并且主要与细胞相关。末端 C5b-9 补体复合物在所有病变中普遍存在。补体调节蛋白和激活产物都仅限于病变涉及的区域，并且在正常动脉壁中不存在。结果表明，参与补体调节和补体配体结合的分子存在于动脉粥样硬化病变中，它们可能发挥调节补体活性的作用。
Complement activation in human atherosclerotic lesions is indicated by the presence of C5b-9 terminal complexes. By using monoclonal antibodies to the complement C3b receptor (CR1) and the iC3b receptor (CR3), it was observed that approximately 20% of the cells in complicated human carotid lesions express CR1 and CR3 antigens. One to five percent of complement receptor-positive cells stained for smooth muscle cell-specific myosin, and the remainder were determined to be predominantly macrophages, based on their reactivity to anti-LeuM3 (CD14) monoclonal antibody. No C3dg receptor (CR2)-positive cells were observed in any of the eight lesions examined. The complement regulatory glycoprotein decay accelerating factor (DAF) was widely distributed extracellularly, in addition to being present on 20% to 60% of the total cell population. Factor H, a plasma protein that regulates alternative pathway C3 convertase formation, was observed extracellularly in 70% of the lesions examined. C1 inhibitor was present in a few plaque specimens, was relatively sparse, and appeared largely cell associated. Terminal C5b-9 complement complexes were pervasive in all lesions. Both the complement regulatory proteins and the activation products were limited to the area of lesion involvement and were absent from normal arterial wall. The results demonstrate that molecules involved in complement regulation and complement ligand binding are present in atherosclerotic lesions, where they may function to modulate the activities of complement.