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“eat-me”信号和自噬货物受体在先天免疫中的作用。

The role of 'eat-me' signals and autophagy cargo receptors in innate immunity.

机构信息

MRC Laboratory of Molecular Biology, Division of Protein and Nucleic Acid Chemistry, Francis Crick Avenue, Cambridge Biomedical Campus, Cambridge CB2 0QH, UK.

出版信息

Curr Opin Microbiol. 2013 Jun;16(3):339-48. doi: 10.1016/j.mib.2013.03.010. Epub 2013 Apr 23.

Abstract

Selective autophagy is an important effector mechanism of cell autonomous immunity, in particular against invasive bacterial species. Anti-bacterial autophagy is activated by rupture of bacteria-containing vacuoles and exposure of bacteria to the cytosol. The autophagy cargo receptors p62, NDP52 and Optineurin detect incoming bacteria that have become associated with specific 'eat-me' signals such as Galectin-8 and poly-ubiquitin and feed them into the autophagy pathway via interactions with phagophore-associated ATG8-like proteins. Here we review recent progress in the field regarding the origin of bacteria-associated 'eat-me' signals, the specific roles of individual cargo receptors and how disrupting cargo receptor function may be important for bacterial evasion of autophagy.

摘要

选择性自噬是细胞自主免疫的一种重要效应机制,特别是针对入侵的细菌种类。抗细菌自噬是通过含菌囊泡的破裂和细菌暴露于细胞质而激活的。自噬货物受体 p62、NDP52 和 Optineurin 检测与特定的“吃我”信号(如半乳糖凝集素-8 和多聚泛素)相关联的已进入的细菌,并通过与吞噬体相关的 ATG8 样蛋白相互作用将其递送入自噬途径。在这里,我们综述了该领域最近的进展,包括与细菌相关的“吃我”信号的起源、各个货物受体的特定作用以及如何破坏货物受体功能可能对细菌逃避自噬很重要。

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