Ligand-induced IFNGR1 down-regulation calibrates myeloid cell IFNγ responsiveness.

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ID: 57745
2019
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Abstract
The type II IFN (IFNγ) enhances antimicrobial activity yet also drives expression of genes that amplify inflammatory responses. Hence, excessive IFNγ stimulation can be pathogenic. Here, we describe a previously unappreciated mechanism whereby IFNγ itself dampens myeloid cell activation. Staining of monocytes from -infected mice provided evidence of type I IFN-independent reductions in IFNGR1. IFNγ was subsequently found to reduce surface IFNGR1 on cultured murine myeloid cells and human CD14 peripheral blood mononuclear cells. IFNγ-driven reductions in IFNGR1 were not explained by ligand-induced receptor internalization. Rather, IFNγ reduced macrophage transcription by altering chromatin structure at putative enhancer sites. This is a distinct mechanism from that used by type I IFNs. Ligand-induced reductions in IFNGR1 altered myeloid cell sensitivity to IFNγ, blunting activation of STAT1 and 3. Our data, thus, reveal a mechanism by which IFNGR1 abundance and myeloid cell sensitivity to IFNγ can be modulated in the absence of type I IFNs. Multiple mechanisms, thus, exist to calibrate macrophage IFNGR1 abundance, likely permitting the fine tuning of macrophage activation and inflammation.
Reference Key
crisler2019ligandinducedlife Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Crisler, William J;Eshleman, Emily M;Lenz, Laurel L;
Journal life science alliance
Year 2019
DOI
e201900447
URL
Keywords
bacteria Machine learning Microbiology tandem mass spectrometry lc-ms/ms urine analysis swath-ms targeted mass spectrometry

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