Division of Infectious Diseases, Department of Medicine, the Pennsylvania State University College of Medicine, Hershey, PA, USA.
Cell Microbiol. 2011 Oct;13(10):1441-50. doi: 10.1111/j.1462-5822.2011.01648.x. Epub 2011 Aug 24.
Plasmodium falciparum malaria is an intracellular parasite that is transmitted by Anopheles mosquitoes. It is responsible for approximately 1 million deaths per year. Most deaths occur as a result of complications such as severe anaemia or cerebral malaria (coma). The complement receptor 1 is a key complement regulator found on the surface of red cells and most leucocytes. A growing body of evidence suggests that this molecule plays a critical role in the pathogenesis of P. falciparum malaria. Initial reports showed that CR1 enables the binding of infected red cells to uninfected red cells to form rosettes, which can potentially obstruct small capillaries. However, further evidence suggests that CR1 is also important in the control of complement activation and immune complex formation during malaria infection. Most recently, CR1 has also been shown to be a receptor for the invasion of red cells by the parasite. Its polymorphic nature almost certainly has allowed the selection of variants that have helped humankind survive the scurge of malaria. The finding of conflicting reports about the exact role of these variants in severe disease underlies the complexity of the parasite-host interactions and highlights the need for further studies.
恶性疟原虫疟疾是一种由疟蚊传播的细胞内寄生虫。它每年导致约 100 万人死亡。大多数死亡是由于严重贫血或脑型疟（昏迷）等并发症引起的。补体受体 1 是一种存在于红细胞和大多数白细胞表面的关键补体调节剂。越来越多的证据表明，该分子在恶性疟原虫疟疾的发病机制中发挥着关键作用。最初的报告表明，CR1 使受感染的红细胞与未受感染的红细胞结合形成玫瑰花结，这可能会阻塞小毛细血管。然而，进一步的证据表明，CR1 在疟疾感染期间控制补体激活和免疫复合物形成方面也很重要。最近，CR1 也被证明是寄生虫入侵红细胞的受体。其多态性几乎肯定允许选择有助于人类在疟疾肆虐中生存的变体。关于这些变体在严重疾病中的确切作用的相互矛盾的报告的发现，说明了寄生虫-宿主相互作用的复杂性，并强调了进一步研究的必要性。
