• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Current opinion in hematology >Modulation of malaria virulence by determinants of Plasmodium falciparum erythrocyte membrane protein-1 display.
【24h】

Modulation of malaria virulence by determinants of Plasmodium falciparum erythrocyte membrane protein-1 display.

机译：恶性疟原虫红细胞膜蛋白-1的决定因素对疟疾毒力的调节。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

PURPOSE OF REVIEW: Plasmodium falciparum malaria parasites carry approximately 60 var genes that encode variable adhesins termed P. falciparum erythrocyte membrane protein-1. Clonal expression of a single P. falciparum erythrocyte membrane protein-1 variant on the surface of the parasitized host erythrocyte promotes binding of the cell to blood elements (including noninfected erythrocytes, leukocytes) and walls of microvessels. These binding events enable parasitized erythrocytes to sequester and avoid clearance by the spleen, and they also contribute to disease by causing microvascular inflammation and obstruction. RECENT FINDINGS: Steps by which P. falciparum erythrocyte membrane protein-1 is exported to the parasitized erythrocyte surface have recently been elucidated. The ability of parasites to cytoadhere and cause disease depends on the variant of P. falciparum erythrocyte membrane protein-1 as well as its amount and distribution at the erythrocyte surface. An example of a host polymorphism that affects P. falciparum erythrocyte membrane protein-1 display is hemoglobin C, which may protect against malaria by impairing the parasite's ability to adhere to microvessels and induce inflammation. Interference with P. falciparum erythrocyte membrane protein-1-mediated phenomena appears to diminish cytoadherence in vivo and to protect against disease in animal models. SUMMARY: Plasmodium falciparum erythrocyte membrane protein-1-mediated sequestration of parasitized erythrocytes plays a central role in malaria pathogenesis. Clinical interventions aimed at reducing cytoadherence and microvascular inflammation may improve disease outcome.
机译：审查的目的：恶性疟原虫疟原虫携带大约60个var基因，它们编码可变的粘附素，称为恶性疟原虫红细胞膜蛋白1。寄生虫宿主红细胞表面上单个恶性疟原虫红细胞膜蛋白-1变体的克隆表达可促进细胞与血液成分（包括未感染的红细胞，白细胞）和微血管壁的结合。这些结合事件使被寄生的红细胞隔离并避免被脾脏清除，它们还通过引起微血管发炎和阻塞而导致疾病。最近的发现：最近已经阐明了恶性疟原虫红细胞膜蛋白1出口到被寄生的红细胞表面的步骤。寄生虫发生细胞粘附并引起疾病的能力取决于恶性疟原虫红细胞膜蛋白-1的变体及其在红细胞表面的数量和分布。影响恶性疟原虫红细胞膜蛋白-1展示的宿主多态性的一个例子是血红蛋白C，它可以通过削弱寄生虫粘附微血管和诱发炎症的能力来预防疟疾。恶性疟原虫红细胞膜蛋白1介导的现象的出现似乎减少了体内的细胞粘附，并在动物模型中预防了疾病。摘要：恶性疟原虫红细胞膜蛋白1介导的寄生性红细胞隔离在疟疾发病机理中起着核心作用。旨在减少细胞粘附和微血管炎症的临床干预措施可能会改善疾病的预后。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号