Horta M F, Ramalho-Pinto F J
Department of Biochemistry-Immunology, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
J Exp Med. 1991 Dec 1;174(6):1399-406. doi: 10.1084/jem.174.6.1399.
Decay-accelerating factor (DAF) is a 70-kD membrane glycoprotein that prevents complement (C)-mediated hemolysis by blocking the assembly or accelerating the decay of C3 convertase. Purified DAF is known to incorporate into the membrane of DAF-deficient cells, inhibiting lysis. Since Schistosoma mansoni is a blood-dwelling parasite, we investigated whether DAF can be transferred from human erythrocytes to the worm and protect it against C-mediated killing in vitro. We have found that schistosomula (schla) incubated with normal human erythrocytes (N-HuE), but not with DAF-deficient erythrocytes, become resistant to C damage in vitro. Protected parasites acquire a 70-kD surface protein which can be immunoprecipitated by anti-DAF antibodies. The acquired resistance is abrogated by treatment of N-HuE-incubated parasites with anti-DAF antibody. These results indicate that, in vitro, N-HuE DAF can be transferred to schla, and suggest its participation in preventing their C-mediated killing. This could represent an important strategy of parasites to evade the host's immune response in vivo.
衰变加速因子（DAF）是一种70kD的膜糖蛋白，它通过阻止补体（C）介导的溶血过程，即阻断C3转化酶的组装或加速其衰变，来防止补体介导的溶血。已知纯化的DAF可整合到缺乏DAF的细胞的膜中，从而抑制细胞裂解。由于曼氏血吸虫是一种寄生于血液中的寄生虫，我们研究了DAF是否能从人红细胞转移到虫体上，并在体外保护其免受补体介导的杀伤。我们发现，与正常人红细胞（N-HuE）孵育的童虫（schla），而不是与缺乏DAF的红细胞孵育的童虫，在体外对补体损伤具有抗性。受保护的寄生虫获得了一种70kD的表面蛋白，该蛋白可被抗DAF抗体免疫沉淀。用抗DAF抗体处理与N-HuE孵育的寄生虫后，所获得的抗性被消除。这些结果表明，在体外，N-HuE的DAF可以转移到童虫上，并提示其参与了防止童虫被补体介导的杀伤。这可能代表了寄生虫在体内逃避宿主免疫反应的一种重要策略。
