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IL-6 induces an anti-inflammatory response in the absence of SOCS3 in macrophages

机译:IL-6在巨噬细胞中不存在SOCS3的情况下诱导抗炎反应

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摘要

Whereas interleukin-6 (IL-6) is a proinflammatory cytokine, IL-10 is an anti-inflammatory cytokine. Although signal transducer and activator of transcription 3 (STAT3) is essential for the function of both IL-6 and IL-10, it is unclear how these two cytokines have such opposing functions. here we show that suppressor of cytokine signaling 3 (SOCS3) is a key regulator of the divergent action of these two cytokines. In macrophages lacking the Scos3 gene or carrying a mutation of the SOCS3-binding site in gp130, the lipopolysaccharide-induced production of tumor necrosis factor (TNF) and IL-12 is suppressed by both IL-10 and IL-6. SOCS3 specifically prevents activation of STAT3 by IL-6 but not IL-10. Taken together, these data indicate that SOCS3 selectively blocks signaling by IL-6, thereby preventing its ability to inhibit LPS signaling.
机译:白介素6(IL-6)是促炎细胞因子,而IL-10是抗炎细胞因子。尽管信号转导和转录激活因子3(STAT3)对于IL-6和IL-10的功能都是必不可少的,但尚不清楚这两种细胞因子如何具有这种相反的功能。在这里,我们显示细胞因子信号传导抑制因子3(SOCS3)是这两种细胞因子的发散作用的关键调节因子。在缺少Scos3基因或gp130中带有SOCS3结合位点突变的巨噬细胞中,IL-10和IL-6均抑制了脂多糖诱导的肿瘤坏死因子(TNF)和IL-12的产生。 SOCS3专门阻止IL-6激活STAT3,但不能阻止IL-10激活。综上所述,这些数据表明SOCS3选择性地阻断IL-6的信号传导,从而阻止其抑制LPS信号传导的能力。

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