NFATC3 promotes IRF7 transcriptional activity in plasmacy--toid dendritic cells

Musheng Bao, York Wang, Ying Liu, Peiqing Shi, Hongbo Lu, Wenwen Sha, Leiyun Weng, Shino Hanabuchi, Jun Qin, Joel Plumas, Laurence Chaperot, Zhiqiang Zhang, Yong-Jun Liu

Research output: Contribution to journalArticle

14 Scopus citations

Abstract

Plasmacytoid dendritic cells (pDCs) rapidly produce large amounts of type 1 interferon (IFN) after Toll-like receptor 7 and 9 engagements. This specialized function of type 1 IFN production is directly linked to the constitutive expression of IRF7, the master transcription factor for type 1 IFN production. However, the IRF7 regulatory network in pDCs remains largely unknown. In this study, we identify that the transcription factor NFATC3 specifically binds to IRF7 and enhances IRF7-mediated IFN production. Furthermore, knockout of NFATC3 greatly reduced the CpG DNA-induced nuclear translocation of IRF7, which resulted in impaired type 1 IFN production in vitro and in vivo. In addition, we found that NFATC3 and IRF7 both bound to type 1 IFN promoters and that the NFAT binding site in IFN promoters was required for IRF7-mediated IFN expression. Collectively, our study shows that the transcription factor NFATC3 binds to IRF7 and functions synergistically to enhance IRF7-mediated IFN expression in pDCs.

Original languageEnglish (US)
Pages (from-to)2383-2398
Number of pages16
JournalThe Journal of experimental medicine
Volume213
Issue number11
DOIs
StatePublished - Oct 17 2016

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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