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- W2951543846 abstract "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 Mycobacterium tuberculosis 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, M. tuberculosis 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 M. tuberculosis 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 M. tuberculosis–mediated inhibition of type I IFN signaling was restricted to infected cells. Overall, our study supports the novel concept that M. tuberculosis evolved to inhibit autocrine type I IFN signaling to evade host defense mechanisms." @default.
- W2951543846 created "2019-06-27" @default.
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- W2951543846 date "2019-04-15" @default.
- W2951543846 modified "2023-09-30" @default.
- W2951543846 title "<i>Mycobacterium tuberculosis</i> Inhibits Autocrine Type I IFN Signaling to Increase Intracellular Survival" @default.
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- W2951543846 doi "https://doi.org/10.4049/jimmunol.1801303" @default.
- W2951543846 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6456408" @default.
- W2951543846 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30833347" @default.
- W2951543846 hasPublicationYear "2019" @default.
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