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Protocol for Production of a Genetic Cross of the Rodent Malaria Parasites
Published on: January 3, 2011
在疟疾中,快速切换到多个抗原和粘合性表型
D J Roberts1, A G Craig, A R Berendt
1Molecular Parasitology Group, Institute of Molecular Medicine, John Radcliffe Hospital, Headington, Oxford, UK.
Nature
|June 25, 1992
概括
严重疟疾的寄生红细胞可以快速改变它们的表面抗原以及它们如何粘附于组织. 这种经常发生的抗原变异会影响疾病的严重程度和免疫反应.
科学领域:
- 疟疾学 疟疾学
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
背景情况:
- 严重的Plasmodium falciparum疟疾病原包括感染的红细胞粘附到内皮和未感染的红细胞.
- 感染的红细胞上的表面新抗原介导着对宿主受体的粘附,并表现出血清学多样性.
- 这些新抗原可能是宿主保护性免疫反应的目标.
研究的目的:
- 研究Plasmodium falciparum寄生虫转换抗原和细胞粘附表型的能力.
- 了解感染红细胞抗原变异的速率和影响.
主要方法:
- 通过微操作对Plasmodium falciparum进行序列克隆.
- 在寄生虫克隆中抗原和粘合性表型切换的体外分析.
主要成果:
- 寄生性红细胞表面抗原在体外以每代2%的速度发生克隆变异,即使没有免疫压力.
- 抗原变异伴随着粘合性表型的同时调制.
- 寄生虫克隆可以切换到各种抗原和粘合性表型,包括感染红细胞的自聚合.
结论:
- 在Plasmodium falciparum中快速的抗原和功能异质性对疟疾病原发生有重大影响.
- 观察到的变异影响了对疟疾的获得免疫力的发展.
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