Regulation of IL-27 p28 gene expression in macrophages through MyD88- and interferon-γ–mediated pathways

Lipopolysaccharides Mice, Knockout 0301 basic medicine Binding Sites DNA, Complementary Base Sequence Interleukins Macrophages Molecular Sequence Data NF-kappa B Articles In Vitro Techniques Mice, Inbred C57BL Interferon-gamma Mice Protein Subunits 03 medical and health sciences Gene Expression Regulation Myeloid Differentiation Factor 88 Animals Female Promoter Regions, Genetic Interferon Regulatory Factor-1
DOI: 10.1084/jem.20061440 Publication Date: 2007-01-17T03:18:44Z
ABSTRACT
Interleukin (IL)-27 is the newest member of IL-12 family heterodimeric cytokines composed Epstein-Barr virus–induced gene 3 and p28 chains. IL-27 not only plays an important role in regulation differentiation naive T helper cells but also possesses antiinflammatory properties. early product activated monocytes/macrophages dendritic cells. However, mechanisms whereby inflammatory signals stimulate production have been explored. In this study, we investigated transcriptional mouse macrophages response to lipopolysaccharide (LPS) interferon (IFN)-γ. We found that LPS-stimulated was completely dependent on Toll-like receptor 4/myeloid factor 88 (MyD88)–mediated pathway partially nuclear κB c-Rel. IFN-γ–induced production/secretion MyD88 independent then cloned promoter mapped its multiple transcription initiation sites. Furthermore, identified critical elements mediate inductive effects LPS IFN-γ, separately synergistically, a c-Rel– regulatory 1–dependent manner, respectively.
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