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IFN-lambda endocytosis and IFN-lambda responsive promoter activation are dependent on cholesterol.

机译:IFN-λ内吞作用和IFN-λ响应性启动子激活取决于胆固醇。

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Recently, a relationship between receptor endocytosis and downstream signaling has been documented for several immunomodulatory molecules. However, endocytosis of interferon-lambdas (IFN-lambdas) and its impact on IFN-lambda function has not been studied. We show that IFN-lambda is internalized through a cholesterol-dependent, dynamin-independent, and Rho family of GTPase-independent pathway in HepG2 cells. Furthermore, we demonstrate that inhibition of IFN-lambda endocytosis by cholesterol depletion suppresses the activation of IFN-lambda responsive promoters. These results suggest that IFN-lambda endocytosis participates in regulating antiviral gene induction and thus may affect antiviral immunity.
机译:最近,对于几种免疫调节分子,已经报道了受体内吞作用和下游信号传导之间的关系。然而,尚未研究干扰素-λ(IFN-λ)的内吞作用及其对IFN-λ功能的影响。我们显示,IFN-lambda通过HepG2细胞中的GTPase依赖性途径的胆固醇依赖性,动力非依赖性和Rho家族而被内化。此外,我们证明通过胆固醇消耗抑制IFN-λ内吞作用可抑制IFN-λ响应性启动子的激活。这些结果表明,IFN-λ内吞作用参与调节抗病毒基因的诱导,因此可能影响抗病毒免疫。

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