PI3K and negative regulation of TLR signaling
PI3K and negative regulation of TLR signaling
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DOI：
10.1016/s1471-4906(03)00139-x
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发表时间：
2003-07-01
影响因子：
16.8
通讯作者：
Koyasu, S
中科院分区：
文献类型：
--
作者：
Fukao, T;Koyasu, S
过度的免疫反应对宿主有害，负反馈调节对于维持免疫系统的完整性至关重要。最近的研究表明，磷脂酰肌醇3-激酶（PI 3 K）是由Toll样受体（TLR）信号触发的白细胞介素-12（IL-12）产生的内源性抑制剂，并限制过度的Th 1极化。与TLR信号传导诱导的IRAK-M（IL-1受体相关激酶-M）和SOCS-1（细胞因子信号传导抑制因子-1）不同，PI 3 K在TLR信号传导的早期阶段发挥作用，并调节初级激活的幅度。因此，PI 3 K，IRAK-M和SOCS-1在守门系统中具有独特的作用，防止过度的先天免疫应答。
Excessive immune responses are detrimental to the host and negative feedback regulation is crucial for the maintenance of immune-system integrity. Recent studies have shown that phosphoinositide 3-kinase (PI3K) is an endogenous suppressor of interleukin-12 (IL-12) production triggered by Toll-like receptor (TLR) signaling and limits excessive Th1 polarization. Unlike IRAK-M (IL-1 receptor-associated kinase-M) and SOCS-1 (suppressor of cytokine signaling-1) that are induced by TLR signaling and function during the second or continuous exposure to stimulation, PI3K functions at the early phase of TLR signaling and modulates the magnitude of the primary activation. Thus, PI3K, IRAK-M and SOCS-1 have unique roles in the gate-keeping system, preventing excessive innate immune responses.