Immunity, Inflammation, and Disease Laboratory, National Institute of Environmental Health Sciences, 111 T.W. Alexander Drive, Research Triangle Park, NC, USA.
Curr Opin Immunol. 2018 Dec;55:54-61. doi: 10.1016/j.coi.2018.09.011. Epub 2018 Oct 2.
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.
溶酶体相关吞噬作用 (LAP) 存在于吞噬作用和自噬这两种进化途径的交汇点。当吞噬细胞吞噬与受体信号结合的细胞外颗粒时，自噬机制的成分和 Rubicon 会被招募到含有货物的吞噬体或 LAPosome 中。LAPosome 的形成对于货物清除以及介导适当的信号级联反应都至关重要。总体而言，LAP 作为一种免疫抑制机制发挥作用，因为 LAP 缺乏通常会导致过度炎症。由于自噬机制的缺陷与异常免疫反应和自身免疫性疾病长期相关，因此现在我们必须重新审视这些关联，将非典型自噬形式（如 LAP）考虑在内。
