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Innate immunity and inflammophagy: balancing the defence and immune homeostasis

期刊

FEBS JOURNAL
卷 289, 期 14, 页码 4112-4131

出版社

WILEY
DOI: 10.1111/febs.16298

关键词

autophagy; inflammation; inflammophagy; innate immunity; noncanonical autophagy; pattern recognition receptor; TRIM proteins; virus

资金

  1. Department of Biotechnology (DBT) EMR grant [BT/PR23942/BRB/10/1808/2019]
  2. Science & Engineering Research Board (SERB) [CRG/2020/003480]
  3. Wellcome Trust/Department of Biotechnology (DBT) India Alliance [IA/I/15/2/502071]
  4. DBT-RA Program in Biotechnology and Life Sciences
  5. DST [DST/INSPIRE/04/2019/001857]

向作者/读者索取更多资源

There is extensive crosstalk between autophagy and innate immune signaling pathways, where increased autophagy aims to eliminate stimuli and regulate inflammatory pathways by targeted degradation of proteins. This interplay helps maintain immune homeostasis and protect against inflammatory and autoimmune diseases. Further systematic studies are needed to fully understand the mechanisms of this interaction.
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.

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