Mycobacterium tuberculosis Inhibits Autocrine Type I IFN Signaling to Increase Intracellular Survival.

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 in

SUBMITTER: Banks DA 

PROVIDER: S-EPMC6456408 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature