General nature of the STAT3-activated anti-inflammatory response
General nature of the STAT3-activated anti-inflammatory response
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DOI：
10.4049/jimmunol.177.11.7880
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发表时间：
2006-12-01
影响因子：
4.4
通讯作者：
Murray, Peter J.
中科院分区：
文献类型：
--
作者：
El Kasmi, Karim C.;Holst, Jeff;Murray, Peter J.
尽管许多细胞因子受体通过STAT 3途径产生其信号，但IL-10 R似乎在通过STAT 3促进有效的抗炎反应（AIR）以拮抗激活先天免疫反应的促炎信号方面是独特的。我们发现，激活STAT 3但对细胞因子信号传导-3介导的抑制的抑制剂天然难治（IL-22 R）或工程化难治（IL-6、瘦素和促红细胞生成素受体）的异源细胞因子受体系统激活与IL-10无区别的AIR。我们的结论是，AIR是一个通用的细胞因子信号通路依赖于STAT 3，但不是唯一的IL-10 R。
Although many cytokine receptors generate their signals via the STAT3 pathway, the IL-10R appears unique in promoting a potent anti-inflammatory response (AIR) via STAT3 to antagonize proinflammatory signals that activate the innate immune response. We found that heterologous cytokine receptor systems that activate STAT3 but are naturally refractory (the IL-22R), or engineered to be refractory (the IL-6, leptin, and erythropoietin receptors), to suppressor of cytokine signaling-3-mediated inhibition activate an AIR indistinguishable from IL-10. We conclude that the AIR is a generic cytokine signaling pathway dependent on STAT3 but not unique to the IL-10R.