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

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ID: 57745
2019
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摘要
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.
参考键
crisler2019ligandinducedlife 使用此键在稿件中自动引用，同时使用 SciMatic 稿件管理器或论文管理器
作者 Crisler, William J;Eshleman, Emily M;Lenz, Laurel L;
期刊 life science alliance
年份 2019
DOI
e201900447
URL
关键词
bacteria Machine learning Microbiology tandem mass spectrometry lc-ms/ms urine analysis swath-ms targeted mass spectrometry

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