Epigenetic and Chromatin Biology Unit, Institute of Life Sciences, Bhubaneswar, India.
Cell Biology and Infectious Diseases Unit, Institute of Life Sciences, Bhubaneswar, Odisha, India.
FEBS J. 2022 Jul;289(14):4112-4131. doi: 10.1111/febs.16298. Epub 2021 Dec 14.
Extensive crosstalk exists between autophagy and innate immune signalling pathways. The stimuli that induce pattern recognition receptor (PRR)-mediated innate immune signalling pathways, also upregulate autophagy. The purpose of this increased autophagy is to eliminate the stimuli and/or suppress the inflammatory pathways by targeted degradation of PRRs or intermediary proteins (termed 'inflammophagy'). By executing these functions, autophagy dampens excess inflammation triggered by the innate immune signalling pathways. Thus, autophagy helps in the maintenance of the body's innate immune homeostasis to protect from inflammatory and autoimmune diseases. Many autophagy-dependent mechanisms that could control innate immune signalling have been studied over the last few years. However, still, the understanding is incomplete, and studies that are more systematic should be undertaken to delineate the mechanisms of inflammophagy. Here, we discuss the available knowledge of crosstalk between autophagy and PRR signalling pathways.
自噬和先天免疫信号通路之间存在广泛的串扰。诱导模式识别受体 (PRR) 介导的先天免疫信号通路的刺激物也会上调自噬。这种自噬增加的目的是通过靶向降解 PRR 或中间蛋白(称为“自噬体”)来消除刺激物和/或抑制炎症途径。通过执行这些功能,自噬可以减轻先天免疫信号通路引发的过度炎症。因此,自噬有助于维持机体先天免疫的内稳态,以防止炎症性和自身免疫性疾病。在过去的几年中,已经研究了许多可以控制先天免疫信号的自噬依赖性机制。然而,目前的理解还不完整,应该进行更系统的研究来阐明自噬体的作用机制。在这里,我们讨论了自噬和 PRR 信号通路之间相互作用的现有知识。