| First Author | Whitley SK | Year | 2018 |
| Journal | J Biol Chem | Volume | 293 |
| Issue | 41 | Pages | 15790-15800 |
| PubMed ID | 30093408 | Mgi Jnum | J:272818 |
| Mgi Id | MGI:6268575 | Doi | 10.1074/jbc.RA118.002721 |
| Citation | Whitley SK, et al. (2018) IL-1R signaling promotes STAT3 and NF-kappaB factor recruitment to distal cis-regulatory elements that regulate Il17a/f transcription. J Biol Chem 293(41):15790-15800 |
| abstractText | Interleukin (IL)-1beta plays a critical role in IL-6beta- and transforming growth factor beta (TGFbeta)-initiated Th17 differentiation and induction of Th17-mediated autoimmunity. However, the means by which IL-1 regulates various aspects of Th17 development remain poorly understood. We recently reported that IL-1beta enhances STAT3 phosphorylation via NF-kappaB-mediated repression of SOCS3 to facilitate Il17 transcription and Th17 differentiation, identifying an effect of IL-1 signaling on proximal events of STAT3 signaling. Here, we show that IL-1beta promotes STAT3 binding to key cis-elements that control IL-17 expression. Additionally, we demonstrate that the IL-1-induced NF-kappaB factor RelA directly regulates the Il17a/f loci in cooperation with STAT3. Our findings reveal that IL-1 impacts both proximal signaling events and downstream interactions between transcription factors and cis-regulatory elements to promote Il17a/f transcription and Th17 differentiation. |
