期刊
JOURNAL OF BIOLOGICAL CHEMISTRY
卷 293, 期 41, 页码 15790-15800出版社
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.RA118.002721
关键词
chromatin immunoprecipitation (ChiP); DNA-protein interaction; NF-kappa B (NF-KB); STAT3; interleukin 17A (IL-17 or IL-17A); interleukin 1 (IL-1)
资金
- National Institutes of Health [R01AI035783, R01DK103744, R01DK115172]
- UAB Medical Scientist Training Program - National Institutes of Health [T32 GM008361]
Interleukin (IL)-1 beta plays a critical role in IL-6-beta- and transforming growth factor beta (TGF beta)-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-1 beta enhances STAT3 phosphorylation via NF-kappa B-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-1 beta promotes STAT3 binding to key cis-elements that control IL-17 expression. Additionally, we demonstrate that the IL-1-induced NF-kappa B 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.
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