Hijacking of host cell IKK signalosomes by the transforming parasite Theileria

Hijacking of host cell IKK signalosomes by the transforming parasite Theileria
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DOI:
10.1126/science.1075462
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发表时间:
2002-11-01
期刊:
影响因子:
56.9
通讯作者:
Dobbelaere, DAE
Dobbelaere, DAE
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Heussler, VT;Rottenberg, S;Dobbelaere, DAE

文献摘要

被引文献

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寄生虫已经进化出了大量的机制来确保它们的繁殖和逃避拮抗宿主的反应。胞内原生动物寄生虫泰勒虫是已知的唯一诱导不受控制的宿主细胞增殖的真核生物。泰勒虫转化的白细胞的存活严格依赖于组成性核因子κ B(NF-κ B)活性。我们发现,这是介导的招聘的多亚基IkappaB激酶(IKK)到大,激活病灶的寄生虫表面。IKK信号体组装是特异性的转化的裂殖体阶段的寄生虫,并下调分化成非转化裂殖子阶段。我们的发现为IKK激活以及病原体如何破坏宿主细胞信号通路提供了见解。
Parasites have evolved a plethora of mechanisms to ensure their propagation and evade antagonistic host responses. The intracellular protozoan parasite Theileria is the only eukaryote known to induce uncontrolled host cell proliferation. Survival of Theileria-transformed leukocytes depends strictly on constitutive nuclear factor kappa B (NF-kappaB) activity. We found that this was mediated by recruitment of the multisubunit IkappaB kinase (IKK) into large, activated foci on the parasite surface. IKK signalosome assembly was specific for the transforming schizont stage of the parasite and was down-regulated upon differentiation into the nontransforming merozoite stage. Our findings provide insights into IKK activation and how pathogens subvert host-cell signaling pathways.