Human high density lipoprotein killing of African trypanosomes.

Human high density lipoprotein killing of African trypanosomes.
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人类高密度脂蛋白杀死非洲锥虫。

DOI:
10.1146/annurev.mi.48.100194.001035
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发表时间:
1994
影响因子:
10.5
通讯作者:
Esko,JD
Esko,JD
中科院分区:
生物学1区
文献类型:
--
作者:
Hajduk,SL;Hager,KM;Esko,JD

文献摘要

被引文献

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由于布鲁氏锥虫对正常人血清的细胞溶解活性敏感,所以它对人类没有传染性。生物化学证据表明,人血清的活性成分是高密度脂蛋白(HDL)。人类HDL杀死锥虫的几种可能机制已经被提出,虽然缺乏一个统一的模型来解释所有的实验信息,但有大量证据表明,受体介导的结合和内吞作用可能需要裂解。抗人类高密度脂蛋白溶解作用的锥虫引起人类昏睡病。这些寄生虫对高密度脂蛋白介导的杀伤产生耐药性的基础尚不清楚。布氏体对人类高密度脂蛋白的细胞溶解作用的敏感性是受发育调控的,耐药性与生物体对大分子摄取的生命周期特异性变化有关。
Trypanosoma brucei brucei is noninfectious to humans because of its sensitivity to the cytolytic activity of normal human serum. Biochemical evidence indicates that the active component of human serum is high-density lipoprotein (HDL). Several possible mechanisms have been proposed for the killing of trypanosomes by human HDL, and while a unified model that accounts for all experimental information is lacking, there is substantial evidence that receptor-mediated binding and endocytosis might be required for lysis. Trypanosomes resistant to the lytic effects of human HDL cause human sleeping sickness. The basis for the resistance of these parasites to HDL-mediated killing is unknown. The sensitivity of T. brucei brucei to the cytolytic action of human HDL is developmentally regulated and resistance correlates with life-cycle specific changes in macromolecular uptake by the organism.