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Overlapping and distinct roles of GRK5 in TLR2-, and TLR3-induced inflammatory response in vivo.

机译:GRK5在TLR2和TLR3诱导的体内炎症反应中的重叠和独特作用。

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G-protein coupled receptor kinase-5 (GRK5) is a recently described NFκB regulator in TLR4 signaling pathway. To determine whether the role of GRK5 is MyD88- or TRIF-dependent, we injected wild type and GRK5 knockout mice with Pam3CSK4 (MyD88-dependent TLR1/2 ligand) and Poly(I:C) (TRIF-dependent TLR3 ligand) and examined the in vivo systemic inflammatory response. Our results demonstrate that GRK5 regulates IL-12p40 and G-CSF via a mechanism that is common to both MyD88 and TRIF. However, GRK5 regulates IL-5 and MCP-1 in a MyD88-dependent but TNFα in a TRIF-dependent manner. Together, our results demonstrate multiple roles of GRK5 in TLR signaling.
机译:G蛋白偶联受体激酶5(GRK5)是TLR4信号通路中最近描述的NFκB调节剂。为了确定GRK5的作用是MyD88依赖性还是TRIF依赖性,我们给野生型和GRK5敲除小鼠注入Pam3CSK4(MyD88依赖性TLR1 / 2配体)和Poly(I:C)(TRIF依赖性TLR3配体)并进行了检查体内全身炎症反应。我们的结果表明,GRK5通过MyD88和TRIF共有的机制调节IL-12p40和G-CSF。但是,GRK5以MyD88依赖性但以TNFα依赖性的方式调节IL-5和MCP-1。总之,我们的结果证明了GRK5在TLR信号传导中的多种作用。

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