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IRF8 and IRF3 cooperatively regulate rapid interferon-β induction in human blood monocytes

Li, Peng, Wong, Joyce Jing-Yi, Sum, Calvin, Sin, Wei-Xiang, Ng, Kok-Quan, Koh, Mickey B. C., Chin, Keh-Chuang·2011·Blood
DOI 10.1182/blood-2010-07-294272
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Abstract

Robust and rapid induction of interferon-β (IFN-β) in monocytes after pathogenic stimulation is a hallmark of innate immune responses. Here, we reveal the molecular mechanism underlying this key property that is exclusive to human blood monocytes. We found that IFN-β was produced rapidly in primary human monocytes as a result of cooperation between the myeloid-specific transcription factor IRF8 and the ubiquitous transcription factor IRF3. Knockdown of IRF8 in monocytes abrogated IFN-β transcription, whereas reintroduction of IRF8 into the IRF8−/− 32Dcl3 murine myeloid cell line reinstated IFN-β transcription. Moreover, we provide evidence that IRF8 constitutively binds to the ETS/IRF composite element of the IFN-β promoter region together with PU.1 in vivo. Furthermore we uncovered a requirement for IRF3, a master regulator of IFN-β production, as a previously un-indentified interaction partner of IRF8. We mapped the protein-protein interacting regions of IRF3 and IRF8, and found that their interaction was independent of the DNA-binding domain and the IRF association domain of IRF8 and IRF3, respectively. Therefore, we propose a model for the rapid induction of IFN-β in monocytes, whereby IRF8 and PU.1 form a scaffold complex on the IFN-β promoter to facilitate the recruitment of IRF3, thus enabling rapid IFN-β transcription.

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Metadata

Authors
Li, P., Wong, J. J.-Y., Sum, C., Sin, W.-X., Ng, K.-Q., Koh, M. B. C., & Chin, K.-C.
Affiliations
  • Laboratory of Gene Regulation and Inflammation, Singapore Immunology Network, Agency for Science, Technology and Research (A*STAR), Biopolis, Immunos #04-00, Singapore;
  • Blood Services Group, Health Sciences Authority, Singapore; and
Venue
Blood
Publisher
American Society of Hematology
Published
2011-03-10
Volume
117
Issue
10
Pages
2847-2854
ISSN
  • 0006-4971
  • 1528-0020
DOI
10.1182/blood-2010-07-294272
Cited by
71
References
5
Language
en

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