title: Innate immune responses regulate morphogenesis and degeneration: roles of Toll-like receptors and Sarm1 in neurons.
abstract: 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.
authors.affiliation: Institute of Molecular Biology, Academia Sinica, Taipei, 115, Taiwan.
authors.forename: Hsin-Yu
authors.initials: HY
authors.lastname: Liu
authors.forename: Chiung-Ya
authors.initials: CY
authors.lastname: Chen
authors.forename: Yi-Ping
authors.initials: YP
authors.lastname: Hsueh
mesh_terms: D000818:Animals; D051186:Armadillo Domain Proteins / Q000378:metabolism*; D001921:Brain / Q000276:immunology; D003598:Cytoskeletal Proteins / Q000378:metabolism*; D006801:Humans; D007113:Immunity, Innate; D051379:Mice; D017628:Microglia / Q000276:immunology; D009024:Morphogenesis / Q000276:immunology*; D009474:Neurons / Q000276:immunology* / Q000473:pathology; D015398:Signal Transduction; D051193:Toll-Like Receptors / Q000378:metabolism*
chemical_list: D051186:Armadillo Domain Proteins; D003598:Cytoskeletal Proteins; C435689:SARM1 protein, human; C543961:SARM1 protein, mouse; D051193:Toll-Like Receptors