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LAP it up, fuzz ball: a short history of LC3-associated phagocytosis

机译:把它伸出,模糊球:LC3相关吞噬作用的短暂历史

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摘要

LC3-associated phagocytosis (LAP) exists at the crossroads of the two evolutionary pathways of phagocytosis and autophagy. When a phagocyte engulfs an extracellular particle that engages receptor signaling, components of the autophagy machinery and Rubicon are recruited to the cargo-containing phagosome or LAPosome. Formation of the LAPosome is critical for both cargo clearance as well as mediating the proper signaling cascade. Globally, LAP functions as an immunosuppressive mechanism, as LAP deficiency often results in hyperinflammation. As defects in the autophagy machinery have been long associated with aberrant immune responses and autoimmune disorders, it is vital that we now revisit these associations with forms of non-canonical autophagy, like LAP, in mind.
机译:LC3相关的吞噬作用(LAP)存在于吞噬作用和自噬的两种进化途径的十字路口。 当吞噬细胞吞噬接合受体信号传导的细胞外颗粒时,募集自噬机械和Rubicon的组分被募集到含货的吞噬体或叶片上。 Laposome的形成对于货物间隙以及调解适当的信号级联来说是至关重要的。 在全球范围内,LAP用作免疫抑制机制,随着LAP缺乏症往往导致高炎症。 随着自噬机械的缺陷长期与异常免疫反应和自身免疫障碍相关,我们现在至关重要,我们现在将这些关联与非规范自噬的形式重新审视如圈子。

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