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凋亡驱动的感染

Apoptosis driven infection.

作者信息

van Zandbergen G, Solbach W, Laskay T

机构信息

Institute for Medical Microbiology and Hygiene, Centre for Structural and Cell Biology in Medicine, University of Lübeck, Lübeck, Germany.

出版信息

Autoimmunity. 2007 Jun;40(4):349-52. doi: 10.1080/08916930701356960.

Abstract

Professional phagocytes like polymorphonuclear neutrophil granulocytes (PMN) and macrophages (MF) kill pathogens as the first line of defense. These cells possess numerous effector mechanisms to eliminate a threat at first contact. However, several microorganisms still manage to evade phagocytic killing, survive and retain infectivity. Some pathogens have developed strategies to silently infect their preferred host phagocytes. The best example of an immune silencing phagocytosis process is the uptake of apoptotic cells. Immune responses are suppressed by the recognition of phosphatidylserine (PS) on the outer leaflet of their plasma membrane. Taking Leishmania major as a prototypic intracellular pathogen, we showed that these organisms can use the apoptotic "eat me" signal PS to silently enter PMN. PS-positive and apoptotic parasites, in an altruistic way, enable the intracellular survival of the viable parasites. Subsequently these pathogens again use PS exposition, now on infected PMN, to silently invade their definitive host cells, the MF. In this review, we will focus on L. major evasion strategies and discuss other pathogens and their use of the apoptotic "eat me" signal PS to establish infection.

摘要

像多形核中性粒细胞(PMN)和巨噬细胞(MF)这样的专业吞噬细胞作为第一道防线杀死病原体。这些细胞拥有众多效应机制,以便在首次接触时消除威胁。然而,仍有几种微生物设法逃避吞噬杀伤,存活并保持传染性。一些病原体已开发出策略来悄悄感染它们偏好的宿主吞噬细胞。免疫沉默吞噬过程的最佳例子是凋亡细胞的摄取。通过识别其质膜外小叶上的磷脂酰丝氨酸(PS)来抑制免疫反应。以杜氏利什曼原虫作为典型的细胞内病原体,我们表明这些生物体可以利用凋亡的“吃我”信号PS悄悄进入PMN。PS阳性和凋亡的寄生虫以利他的方式使活的寄生虫在细胞内存活。随后,这些病原体再次利用现在感染的PMN上的PS暴露,悄悄侵入它们的终末宿主细胞MF。在这篇综述中,我们将重点关注杜氏利什曼原虫的逃避策略,并讨论其他病原体以及它们如何利用凋亡的“吃我”信号PS来建立感染。

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