贝西金是一种受体,对红细胞被Plasmodium falciparum入侵至关重要
Cécile Crosnier1, Leyla Y Bustamante, S Josefin Bartholdson
1Cell Surface Signalling Laboratory, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1HH, UK.
Nature
|November 15, 2011
概括
科学家发现,Plasmodium falciparum疟疾寄生虫需要基因受体和PfRh5连接体,以在所有菌株中进行红细胞入侵. 这种基本的相互作用为新的抗疟疾疗法提供了一个有希望的目标.
科学领域:
- 疟疾学 疟疾学
- 寄生虫学的寄生虫学
- 分子和细胞生物学分子和细胞生物学
背景情况:
- 红细胞被Plasmodium falciparum入侵对于疟疾的发病过程至关重要.
- 现有知识表明,不同的寄生虫菌株使用多个多余的入侵途径.
- 在所有P. falciparum菌株中,没有单个受体-连接体相互作用被确定为必不可少的.
研究的目的:
- 在所有测试的菌株中识别一种对于P. falciparum红细胞入侵至关重要的受体-连接体对.
- 研究巴西金和PfRh5在疟疾寄生虫入侵机制中的作用.
- 探索疟疾潜在的新治疗点.
主要方法:
- 系统选红细胞蛋白来识别寄生虫配体的受体.
- 使用可溶性巴西金,巴西金抗击剂和抗巴西金抗体来抑制入侵的功能性测试.
- 对OK(a-) 红细胞具有改变基因结合亲和力的侵袭效率的分析.
主要成果:
- 鉴定了巴西金 (OK血型抗原) 作为P. falciparum连接体PfRh5.5的基本受体.
- 在所有测试的菌株中,通过可溶性巴西金,巴西金敲击和抗巴西金抗体,证明了红细胞入侵的强有力的抑制.
- 由于PfRh5结合较弱,观察到Ok(a-) 红细胞的侵入效率降低.
结论:
- PfRh5基因相互作用是P. falciparum红细胞入侵的跨菌株必不可少的途径.
- 这种保存的受体-连接体对是开发广谱抗疟疾药物的非常有前途的目标.
- 针对这种相互作用可以克服与冗余入侵途径相关的抵抗机制.
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