Baranyi L, Okada N, Baranji K, Takizawa H, Okada H
Department of Molecular Biology, Nagoya City University School of Medicine, Japan.
Clin Exp Immunol. 1994 Oct;98(1):134-9. doi: 10.1111/j.1365-2249.1994.tb06619.x.
Decay accelerating factor (DAF), membrane cofactor protein (MCP), complement receptor 1 and mouse Crry are cell surface-bound complement regulatory proteins capable of inhibiting C3 convertase activity on cell membranes, and therefore provide a substantial protection from attack by homologous complement activated either by the classical or by the alternative pathway. Decrease in complement regulatory activity might lead to spontaneous complement deposition and subsequent cell injury. MoAb 5I2 can inhibit the complement regulatory activity of molecules on rat cells, resulting in deposition of homologous complement. The antigen recognized by 5I2 MoAb in rats is homologous to mouse Crry. Fifteen to 20 h after infection with vaccinia virus, in vitro cultured KDH-8 rat hepatoma cells show a strong decrease in expression of Crry-like antigen, and proved to be sensitive to complement deposition when 1:5 diluted normal rat serum was added to the culture medium as a source of complement. Addition of complement to the cultured KDH-8 cells infected with a very low dose of vaccinia virus (1 plaque-forming unit (PFU)/1000 cells) substantially reduced spreading of virus infection in the cell culture, while inactivation of complement by heat or zymosan treatment abrogated the protective effect.
衰变加速因子（DAF）、膜辅因子蛋白（MCP）、补体受体1和小鼠Crry是细胞表面结合的补体调节蛋白，能够抑制细胞膜上的C3转化酶活性，因此能为细胞提供重要保护，使其免受经典途径或替代途径激活的同源补体的攻击。补体调节活性降低可能导致补体自发沉积并随后造成细胞损伤。单克隆抗体5I2可抑制大鼠细胞上分子的补体调节活性，导致同源补体沉积。5I2单克隆抗体在大鼠中识别的抗原与小鼠Crry同源。在用痘苗病毒感染15至20小时后，体外培养的KDH-8大鼠肝癌细胞显示Crry样抗原的表达大幅下降，并且当向培养基中添加1:5稀释的正常大鼠血清作为补体来源时，证明其对补体沉积敏感。向感染极低剂量痘苗病毒（1个空斑形成单位（PFU）/1000个细胞）的KDH-8培养细胞中添加补体，可显著减少病毒感染在细胞培养物中的扩散，而通过加热或酵母聚糖处理使补体失活则可消除这种保护作用。
