毒素可以通过注入多态激酶同类物来选择宿主基因表达
J P J Saeij1, S Coller, J P Boyle
1Department of Microbiology and Immunology, Fairchild Building D305, 300 Pasteur Drive, Stanford University School of Medicine, Stanford, California 94305-5124, USA.
Nature
|December 22, 2006
概括
东道细胞操纵中的Toxoplasma gondii菌株差异是由于ROP16蛋白激酶. 这种寄生虫蛋白质会影响宿主转录和互白素-12的产生,影响感染的结果.
科学领域:
- 寄生虫学的寄生虫学
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
背景情况:
- 毒素菌,一个Apicomplexa寄生虫,在免疫受损的个体中引起严重疾病.
- 感染结果和体外生长在T. gondii菌株之间存在显著差异.
- 了解菌株特异性宿主寄生虫相互作用对于疾病管理至关重要.
研究的目的:
- 为了研究托克索普拉斯马淋巴菌对宿主细胞转录的调节的菌株特异性差异的分子机制.
- 为了确定寄生虫因子,负责对宿主信号通路的差异性影响.
- 为了阐明T. gondii血统是如何发展出不同的宿主利用策略的.
主要方法:
- 在II型和III型T. gondii线之间进行遗传交叉.
- 在寄生虫入侵后对宿主细胞转录的分析.
- 调查鱼蛋白 ROP16 在宿主细胞信号传递中的作用.
- 评估对信号传感器和转录激活器 (STAT) 途径和互白素-12 (IL-12) 生产的影响.
主要成果:
- 宿主细胞转录调节的菌株特异性差异是由蛋白质激酶 ROP16 介导的.
- 在侵袭后,ROP16从罗普特里斯中释放出来,并注入宿主细胞.
- ROP16影响STAT信号通路和下游IL-12的产生.
- 第二类和第三类菌株表现出明显的ROP16多态,影响宿主相互作用.
结论:
- ROP16是一种关键的毒性因子,在T. gondii中调解菌株特异性宿主免疫逃避.
- 这项研究揭示了一种新的宿主-寄生虫相互作用机制,涉及对宿主转录的有针对性的调节.
- 在ROP16功能上的差异突出了T. gondii血统开发的战略,以利用宿主环境.
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