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Inhibits Autocrine Type I IFN Signaling to Increase Intracellular Survival. | LitMetric

AI Article Synopsis

Article Abstract

The type I IFNs (IFN-α and -β) are important for host defense against viral infections. In contrast, their role in defense against nonviral pathogens is more ambiguous. In this article, we report that IFN-β signaling in murine bone marrow-derived macrophages has a cell-intrinsic protective capacity against via the increased production of NO. The antimycobacterial effects of type I IFNs were mediated by direct signaling through the IFN-α/β-receptor (IFNAR), as Ab-mediated blocking of IFNAR1 prevented the production of NO. Furthermore, is able to inhibit IFNAR-mediated cell signaling and the subsequent transcription of 309 IFN-β-stimulated genes in a dose-dependent way. The molecular mechanism of inhibition by involves reduced phosphorylation of the IFNAR-associated protein kinases JAK1 and TYK2, leading to reduced phosphorylation of the downstream targets STAT1 and STAT2. Transwell experiments demonstrated that the -mediated inhibition of type I IFN signaling was restricted to infected cells. Overall, our study supports the novel concept that evolved to inhibit autocrine type I IFN signaling to evade host defense mechanisms.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6456408PMC
http://dx.doi.org/10.4049/jimmunol.1801303DOI Listing

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