| First Author | Pattison MJ | Year | 2013 |
| Journal | FEBS Lett | Volume | 587 |
| Issue | 10 | Pages | 1496-503 |
| PubMed ID | 23542035 | Mgi Jnum | J:197246 |
| Mgi Id | MGI:5491967 | Doi | 10.1016/j.febslet.2013.03.025 |
| Citation | Pattison MJ, et al. (2013) IFNbeta autocrine feedback is required to sustain TLR induced production of MCP-1 in macrophages. FEBS Lett 587(10):1496-503 |
| abstractText | Chemokines, including MCP-1, are crucial to mounting an effective immune response due to their ability to recruit other immune cells. We show that sustained LPS or poly(I:C)-stimulated MCP-1 production requires an IFNbeta-mediated feedback loop. Consistent with this, exogenous IFNbeta was able to induce MCP-1 transcription in the absence of other stimuli. Blocking IFNbeta signaling with Ruxolitinib, a JAK inhibitor, inhibited MCP-1 transcription. The MCP-1 promoter contains potential STAT binding sites and we demonstrate that STAT1 is recruited upon IFNbeta stimulation. Furthermore we find that IL-10 knockout increases MCP-1 production in response to LPS, which may reflect an ability of IL-10 to repress IFNbeta production. Overall, these results show the importance of the balance between IFNbeta and IL-10 in the regulation of MCP-1. |
