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The Cross-Regulation Between Autophagy and Type I Interferon Signaling in Host Defense

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Autophagy Regulation of Innate Immunity

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 1209))

Abstract

The production of type I interferons (IFNs) is one of the hallmarks of intracellular antimicrobial program. Typical type I IFN response activates the Janus kinase (JAK)–signal transducer and activator of transcription (STAT) pathway, which results in the transcription of plentiful IFN-stimulated genes (ISGs) to establish the comprehensive antiviral states. Type I IFN signaling should initiate timely to provoke innate and adaptive immune responses for effective elimination of the invading pathogens. Meanwhile, a precise control must come on the stage to restrain the persistent activation of type I IFN responses to avoid attendant toxicity. Autophagy, a conserved eukaryotic degradation system, mediated by a number of autophagy-related (ATG) proteins, plays an essential role in the clearance of invading microorganism and manipulation of type I responses. Autophagy modulates type I IFN responses through regulatory integration with innate immune signaling pathways, and by removing endogenous ligands of innate immune sensors. Moreover, selective autophagy governs the choice of innate immune factors as specific cargoes for degradation, thus tightly monitoring the type I IFN responses. This review will focus on the cross-regulation between autophagy and type I IFN signaling in host defense.

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Acknowledgements

This work was supported by the National Natural Science Foundation of China (31970700 and 31700760) and the Fundamental Research Funds for the Central Universities (18lgpy49).

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Correspondence to Shouheng Jin .

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Jin, S. (2019). The Cross-Regulation Between Autophagy and Type I Interferon Signaling in Host Defense. In: Cui, J. (eds) Autophagy Regulation of Innate Immunity. Advances in Experimental Medicine and Biology, vol 1209. Springer, Singapore. https://doi.org/10.1007/978-981-15-0606-2_8

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