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Innate immune responses regulate morphogenesis and degeneration: roles of Toll-like receptors and Sarm1 in neurons

机译:先天性免疫反应调节形态发生和变性:Toll样受体和Sarm1在神经元中的作用。

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摘要

The central nervous system is recognized as an immunoprivileged site because peripheral immune cells do not typically enter it. Microglial cells are thought to be the main immune cells in brain. However, recent reports have indicated that neurons express the key players of innate immunity, including Toll-like receptors (TLRs) and their adaptor proteins (Sarm1, Myd88, and Trif), and may produce cytokines in response to pathogen infection. In the absence of an immune challenge, neuronal TLRs can detect intrinsic danger signals and modulate neuronal morphology and function. In this article, we review the recent findings on the involvement of TLRs and Sarm1 in controlling neuronal morphogenesis and neurodegeneration. Abnormal behaviors in TLR- and Sarm1-deficient mice are also discussed.
机译:由于周围的免疫细胞通常不进入中枢神经系统,因此它被认为是免疫特权的部位。小胶质细胞被认为是大脑中的主要免疫细胞。但是,最近的报道表明,神经元表达先天免疫的关键参与者,包括Toll样受体(TLR)及其衔接蛋白(Sarm1,Myd88和Trif),并且可能会响应病原体感染而产生细胞因子。在没有免疫攻击的情况下,神经元TLR可以检测内在的危险信号并调节神经元的形态和功能。在本文中,我们回顾了有关TLR和Sarm1参与控制神经元形态发生和神经变性的最新发现。还讨论了在TLR和Sarm1缺陷小鼠中的异常行为。

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