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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Suppressor of cytokine signaling-1 selectively inhibits LPS-induced IL-6 production by regulating JAK-STAT.
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Suppressor of cytokine signaling-1 selectively inhibits LPS-induced IL-6 production by regulating JAK-STAT.

机译：细胞因子信号通路1的抑制剂通过调节JAK-STAT选择性抑制LPS诱导的IL-6产生。

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摘要

Suppressor of cytokine signaling-1 (SOCS-1) is one of the negative-feedback regulators of Janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling. We previously showed that SOCS-1 participates in LPS signaling, but it is not entirely clear yet how SOCS-1 suppresses LPS signaling. In this study, we demonstrate that SOCS-1 selectively inhibits LPS-induced IL-6 production through regulation of JAK-STAT but not production of TNF-alpha, granulocyte colony-stimulating factor, IFN-beta, and other cytokines. We found that LPS directly activated Jak2 and Stat5, whereas SOCS-1 inhibited LPS-induced Jak2 and Stat5 activation. Furthermore, AG490, a Jak-specific inhibitor, and dominant negative Stat5 only reduced LPS-induced IL-6 production. Additionally, Stat5 interacted with p50, resulting in recruitment of Stat5 to the IL-6 promoter together with p50 in response to LPS stimulation. These findings suggest that the JAK-STAT pathway participates in LPS-induced IL-6 production and that SOCS-1 suppresses LPS signaling by regulating JAK-STAT.
机译：细胞因子信号传导抑制因子1（SOCS-1）的抑制是Janus激酶（JAK）信号传导和转录激活因子（STAT）的负反馈调节因子之一。我们之前已经证明SOCS-1参与LPS信号传导，但是尚不清楚SOCS-1如何抑制LPS信号传导。在这项研究中，我们证明SOCS-1通过调节JAK-STAT选择性抑制LPS诱导的IL-6产生，但不抑制TNF-α，粒细胞集落刺激因子，IFN-β和其他细胞因子的产生。我们发现LPS直接激活Jak2和Stat5，而SOCS-1抑制LPS诱导的Jak2和Stat5激活。此外，Jak特异性抑制剂AG490和显性阴性Stat5仅降低LPS诱导的IL-6产生。另外，Stat5与p50相互作用，导致响应LPS刺激，Stat5与p50一起募集到IL-6启动子。这些发现表明，JAK-STAT途径参与LPS诱导的IL-6产生，SOCS-1通过调节JAK-STAT抑制LPS信号传导。

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