期刊
CYTOKINE & GROWTH FACTOR REVIEWS
卷 44, 期 -, 页码 11-17出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.cytogfr.2018.10.003
关键词
Interferon; IRF; STAT; Chromatin; Transcription; Antiviral; NF kappa B
资金
- NIH [GM111652]
- NIH Viral Replication Training Grant [5T32AI060523-07]
- John N. Nicholson Fellowship
In response to virus infections, a cell-autonomous, transcription-based antiviral program is engaged to create resistance, impair pathogen replication, and alert professional cells in innate and adaptive immunity. This dual phase antiviral program consists of type I interferon (IFN) production followed by the response to IFN signaling. Pathogen recognition leads to activation of IRF and NF kappa B factors that function independently and together to recruit cellular coactivators that remodel chromatin, modify histones and activate RNA polymerase II (Pol II) at target gene loci, including the well-characterized IFN beta enhanceosome. In the subsequent response to IFN, a receptor-mediated JAK-STAT signaling cascade directs the assembly of the IRF9-STAT1-STAT2 transcription factor complex called ISGF3, which recruits its own cohort of remodelers, coactivators, and Pol II machinery to activate transcription of a wide range of IFN-stimulated genes. Regulation of the IFN and antiviral gene regulatory networks is not only important for driving innate immune responses to infections, but also may inform treatment of a growing list of chronic diseases that are characterized by hyperactive and constitutive IFN and IFN-stimulated gene (ISG) expression. Here, gene-specific and genome-wide investigations of the chromatin landscape at IFN and ISGs is discussed in parallel with IRF- and STAT-dependent regulation of Pol II transcription.
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