LC3-associated phagocytosis at a glance
LC3-associated phagocytosis at a glance
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DOI：
10.1242/jcs.222984
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发表时间：
2019-03-01
影响因子：
4
通讯作者：
Green, Douglas R.
中科院分区：
文献类型：
--
作者：
Heckmann, Bradlee L.;Green, Douglas R.
经典的自噬被认为是一种响应营养不足而启动的生存机制。我们现在了解到，自噬在多种情况下发挥作用，需要维持体内平衡。最近的证据表明，自噬蛋白的各种非规范功能在机制和功能上与自噬不同。LC 3相关的吞噬作用（LC 3-associated phagocytosis，简称PHG）是自噬蛋白的一种新功能，是各种细胞和组织类型的免疫调节和炎症反应的贡献者。以LC 3家族蛋白与吞噬体膜的缀合为特征，在识别包括病原体、垂死细胞、可溶性配体和蛋白质聚集体在内的各种货物的表面受体的连接之后，噬菌体使用一部分典型的自噬机制。然而，在体内操纵β-淀粉样蛋白途径改变了免疫激活和炎症反应，而不是影响典型的自噬。在这篇《细胞科学一瞥》文章和随附的海报中，我们通过比较和对比每种途径的共享和独特组分，详细介绍了这种独特机制与经典自噬机制的差异。
Classically, canonical autophagy has been considered a survival mechanism initiated in response to nutrient insufficiency. We now understand that autophagy functions in multiple scenarios where it is necessary to maintain homeostasis. Recent evidence has established that a variety of non-canonical functions for autophagy proteins are mechanistically and functionally distinct from autophagy. LC3-associated phagocytosis (LAP) is one such novel function for autophagy proteins and is a contributor to immune regulation and inflammatory responses across various cell and tissue types. Characterized by the conjugation of LC3 family proteins to phagosome membranes, LAP uses a portion of the canonical autophagy machinery, following ligation of surface receptors that recognize a variety of cargos including pathogens, dying cells, soluble ligands and protein aggregates. However, instead of affecting canonical autophagy, manipulation of the LAP pathway in vivo alters immune activation and inflammatory responses. In this Cell Science at a Glance article and the accompanying poster, we detail the divergence of this distinctive mechanism from that of canonical autophagy by comparing and contrasting shared and unique components of each pathway.