Liu Hsin-Yu, Chen Chiung-Ya, Hsueh Yi-Ping
Institute of Molecular Biology, Academia Sinica, Taipei, 115, Taiwan.
Neurosci Bull. 2014 Aug;30(4):645-54. doi: 10.1007/s12264-014-1445-5. Epub 2014 Jul 4.
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.
中枢神经系统被认为是一个免疫特惠部位,因为外周免疫细胞通常不会进入其中。小胶质细胞被认为是大脑中的主要免疫细胞。然而,最近的报道表明,神经元表达先天免疫的关键因子,包括Toll样受体(TLRs)及其衔接蛋白(Sarm1、Myd88和Trif),并且可能在病原体感染时产生细胞因子。在没有免疫挑战的情况下,神经元TLRs可以检测内在危险信号并调节神经元形态和功能。在本文中,我们综述了TLRs和Sarm1在控制神经元形态发生和神经退行性变方面的最新研究结果。还讨论了TLR和Sarm1缺陷小鼠的异常行为。