The Interplay Between Pattern Recognition Receptors and Autophagy in Inflammation.

Abstract

Pattern recognition receptors (PRRs) are sensors of exogenous and endogenous "danger" signals from pathogen-associated molecular patterns (PAMPs), and damage associated molecular patterns (DAMPs), while autophagy can respond to these signals to control homeostasis. Almost all PRRs can induce autophagy directly or indirectly. Toll-like receptors (TLRs), Nod-like receptors (NLRs), retinoic acid-inducible gene-I-like receptors (RLRs), and cyclic guanosine monophosphate-adenosine monophosphate synthase (cGAS)-stimulator of interferon genes (STING) pathway can induce autophagy directly through Beclin-1 or LC3-dependent pathway, while the interactions with the receptor for advanced glycation end products (RAGE)/high mobility group box 1 (HMGB1), CD91/Calreticulin, and TLRs/HSPs are achieved by protein, Ca2+, and mitochondrial homeostasis. Autophagy presents antigens to PRRs and helps to clean the pathogens. In addition, the induced autophagy can form a negative feedback regulation of PRRs-mediated inflammation in cell/disease-specific manner to maintain homeostasis and prevent excessive inflammation. Understanding the interaction between PRRs and autophagy in a specific disease will promote drug development for immunotherapy. Here, we focus on the interactions between PRRs and autophagy and how they affect the inflammatory response.

• Authors: Yun Zhu, Jian Deng, Mei-Ling Nan, Jing Zhang, Akinkunmi Okekunle, Jiang-Yuan Li, Xiao-Qiang Yu, Pei-Hui Wang
• Journal: Advances in experimental medicine and biology (Adv Exp Med Biol) Vol. 1209 Pg. 79-108 ( 2019) ISSN: 0065-2598 [Print] United States
• PMID: 31728866 (Publication Type: Journal Article, Review)

Chemical References

• Receptors, Pattern Recognition

Topics

• Autophagy (immunology)
• Humans
• Inflammation
• Receptors, Pattern Recognition (metabolism)
• Signal Transduction