期刊
FEBS LETTERS
卷 587, 期 10, 页码 1496-1503出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.febslet.2013.03.025
关键词
MCP-1; IL-10; MAPK; TLR; Signaling
资金
- MRC
- Wellcome Trust [087079/Z/08/Z]
- AstraZeneca
- Boehringer-Ingelheim
- GlaxoSmithKline
- Merck KgaA
- JanssenPharmaceutica
- Pfizer
- Medical Research Council [999692, MC_U127081014, MC_UU_12016/10] Funding Source: researchfish
- MRC [MC_UU_12016/10, MC_U127081014] Funding Source: UKRI
- Wellcome Trust [087079/Z/08/Z] Funding Source: Wellcome Trust
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 IFN beta-mediated feedback loop. Consistent with this, exogenous IFN beta was able to induce MCP-1 transcription in the absence of other stimuli. Blocking IFN beta 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 IFNb 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 IFN beta production. Overall, these results show the importance of the balance between IFN beta and IL-10 in the regulation of MCP-1.
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