SOCS-1 participates in negative regulation of LPS responses
SOCS-1 participates in negative regulation of LPS responses
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DOI：
10.1016/s1074-7613(02)00449-1
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发表时间：
2002-11-01
期刊：
影响因子：
32.4
通讯作者：
Kishimoto, T
中科院分区：
文献类型：
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作者：
Nakagawa, R;Naka, T;Kishimoto, T
SOCS-1是JAK-STAT信号级联的负调控分子。在这里，我们证明了SOCS-1是LPS信号通路的关键下调因子。在LPS刺激后，在巨噬细胞中迅速诱导SOCS-1表达。SOCS 1缺陷小鼠对LPS诱导的休克高度敏感，并产生增加的炎性细胞因子水平。SOCS-1的引入抑制了LPS诱导的巨噬细胞中NF-κ B和STAT 1的活化。此外，在SOCS（-1-）缺陷小鼠中未观察到LIPS耐受性（对第二次LPS刺激的不应状态）。这些结果表明，SOCS-1作为一个重要的，负调节LPS反应，保护主机从有害的过度反应LPS，并可能提供新的见解内毒素诱导的致命综合征，偶尔发生感染后。
SOCS-1 is a negative regulatory molecule of the JAK-STAT signal cascade. Here, we demonstrate that SOCS-1 is a critical downregulating factor for LPS signal pathways. SOCS-1 expression was promptly induced in macrophages upon LPS stimulation. SOCS1-deficient mice were highly sensitive to LPS-induced shock and produced increased levels of inflammatory cytokines. Introduction of SOCS-1 inhibited LPS-induced NF-kappaB and STAT1 activation in macrophages. Furthermore, LIPS tolerance, a refractory state to second LPS stimulation, was not observed in SOCS(-1-)deficient mice. These results suggest SOCS-1 as an essential, negative regulator in LPS responses that protects the host from harmful overresponses to LPS and may provide new insight into the endotoxin-induced fatal syndrome that occasionally occurs following infection.