Kinoshita T, Medof M E, Nussenzweig V
J Immunol. 1986 May 1;136(9):3390-5.
Decay-accelerating factor (DAF) is a membrane glycoprotein found on various cells that are in contact with complement. It inhibits the formation of the C3 convertases of the complement system, both the classic (C4b2a) and alternative (C3bBb) pathways. In this investigation, we used a homobifunctional cross-linking reagent to search for a DAF ligand on the surface of cells subjected to complement attack. We found that DAF forms complexes with C4b and C3b deposited on the same erythrocytes, but not with the physiologic degradation products of these complement fragments, that is, C4d or C3dg. Taken together with prior observations that DAF action is reversible, and DAF does not affect the structure of C4b or C3b, these findings suggest that DAF functions by competitively inhibiting the uptake of C2 or factor B, and preventing the assembly of the C3 convertases.
衰变加速因子（DAF）是一种在与补体接触的各种细胞上发现的膜糖蛋白。它抑制补体系统经典途径（C4b2a）和替代途径（C3bBb）中C3转化酶的形成。在本研究中，我们使用同双功能交联剂在遭受补体攻击的细胞表面寻找DAF配体。我们发现DAF与沉积在同一红细胞上的C4b和C3b形成复合物，但不与这些补体片段的生理性降解产物即C4d或C3dg形成复合物。结合先前关于DAF作用是可逆的且DAF不影响C4b或C3b结构的观察结果，这些发现表明DAF通过竞争性抑制C2或B因子的摄取以及阻止C3转化酶的组装来发挥作用。
