Asch A S, Kinoshita T, Jaffe E A, Nussenzweig V
J Exp Med. 1986 Jan 1;163(1):221-6. doi: 10.1084/jem.163.1.221.
Decay-accelerating factor (DAF) has been previously described only in cells of bone marrow origin where it serves as a negative modulator of complement activation. Using mAb against human DAF, we demonstrated the presence of DAF in human umbilical vein endothelial cells by immunofluorescence microscopy and flow cytometry. By means of an immunoradiometric assay we detected an average of 3.3 X 10(5) molecules of DAF on each cell. When immunoisolates were analyzed in Western blots, endothelial cell DAF comigrated with DAF purified from normal erythrocytes. DAF was synthesized by the endothelial cells since 35S-labeled DAF could be immunoisolated from HUVEC cultured in medium containing [35S]methionine. This is the first evidence for the presence of DAF in cells of extra-marrow origin. DAF may protect endothelial cells from complement-mediated injury.
衰变加速因子（DAF）此前仅在骨髓来源的细胞中被描述，在这些细胞中它作为补体激活的负调节因子。使用抗人DAF的单克隆抗体，我们通过免疫荧光显微镜和流式细胞术证明了人脐静脉内皮细胞中存在DAF。通过免疫放射分析，我们检测到每个细胞平均有3.3×10⁵个DAF分子。当在蛋白质印迹中分析免疫分离物时，内皮细胞DAF与从正常红细胞中纯化的DAF迁移情况相同。DAF是由内皮细胞合成的，因为可以从在含有[³⁵S]甲硫氨酸的培养基中培养的人脐静脉内皮细胞（HUVEC）中免疫分离出³⁵S标记的DAF。这是首次证明在骨髓外来源的细胞中存在DAF。DAF可能保护内皮细胞免受补体介导的损伤。
