Wiesner J, Jomaa H, Wilhelm M, Tony H P, Kremsner P G, Horrocks P, Lanzer M
Zentrum für Infektionsforschung, Universität Würzburg, Germany.
Eur J Immunol. 1997 Oct;27(10):2708-13. doi: 10.1002/eji.1830271034.
Here we demonstrate that components of the entire complement cascade are fixed on the surface of erythrocytes infected with the human malarial parasite Plasmodium falciparum. Despite the activation of lytic complement factors, no complement-mediated lysis of P. falciparum-infected erythrocytes occurred only in the absence of functional intrinsic CD59. These data suggest that the restriction of the complement attack of P. falciparum-infected erythrocytes is principally mediated by intrinsic host cell factors, in particular CD59.
在此我们证明，整补体级联反应的成分固定在感染人类疟原虫恶性疟原虫的红细胞表面。尽管溶解补体因子被激活，但仅在缺乏功能性内在CD59时，才未发生补体介导的恶性疟原虫感染红细胞的溶解。这些数据表明，恶性疟原虫感染红细胞的补体攻击受限主要由内在宿主细胞因子介导，尤其是CD59。
