| First Author | Bao M | Year | 2016 |
| Journal | J Exp Med | Volume | 213 |
| Issue | 11 | Pages | 2383-2398 |
| PubMed ID | 27697837 | Mgi Jnum | J:237414 |
| Mgi Id | MGI:5812724 | Doi | 10.1084/jem.20160438 |
| Citation | Bao M, et al. (2016) NFATC3 promotes IRF7 transcriptional activity in plasmacy--toid dendritic cells. J Exp Med 213(11):2383-2398 |
| abstractText | 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. |
