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Apoptotic mimicry as a strategy for the establishment of parasitic infections: parasite- and host-derived phosphatidylserine as key molecule.
Cell Communication and Signaling ( IF 8.2 ) Pub Date : 2020-01-15 , DOI: 10.1186/s12964-019-0482-8
João Luiz Mendes Wanderley 1 , Renato Augusto DaMatta 2 , Marcello André Barcinski 3
Affiliation  

The establishment of parasitic infection is dependent on the development of efficient strategies to evade the host defense mechanisms. Phosphatidylserine (PS) molecules are pivotal for apoptotic cell recognition and clearance by professional phagocytes. Moreover, PS receptors are able to trigger anti-inflammatory and immunosuppressive responses by phagocytes, either by coupled enzymes or through the induction of regulatory cytokine secretion. These PS-dependent events are exploited by parasites in a mechanism called apoptotic mimicry. Generally, apoptotic mimicry refers to the effects of PS recognition for the initiation and maintenance of pathogenic infections. However, in this context, PS molecules can be recognized on the surface of the infectious agent or in the surface of apoptotic host debris, leading to the respective denomination of classical and non-classical apoptotic mimicry. In this review, we discuss the role of PS in the pathogenesis of several human infections caused by protozoan parasites. Video Abstract.

中文翻译:

凋亡模拟作为建立寄生虫感染的策略:寄生虫和宿主来源的磷脂酰丝氨酸是关键分子。

寄生虫感染的建立取决于制定有效策略以规避宿主防御机制。磷脂酰丝氨酸(PS)分子对于凋亡细胞的识别和专业吞噬细胞的清除至关重要。此外,PS受体能够通过吞噬细胞,通过偶联酶或通过诱导调节性细胞因子分泌来触发抗炎和免疫抑制反应。这些依赖于PS的事件被寄生虫以一种称为细胞凋亡模仿的机制利用。通常,细胞凋亡模拟是指PS识别对于引发和维持病原性感染的作用。但是,在这种情况下,PS分子可以在传染原表面或凋亡宿主残骸表面被识别,导致经典和非经典凋亡模拟的名称。在这篇综述中,我们讨论了PS在由原生动物寄生虫引起的几种人类感染的发病机理中的作用。录像摘要。
更新日期:2020-01-15
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