Toll-like receptor 2 signaling in response to brain injury: an innate bridge to neuroinflammation.

摘要: Reactive gliosis is a prominent feature of neurodegenerative and neuroinflammatory disease in the CNS, yet stimuli that drive this response are not known. There growing appreciation signaling through Toll-like receptors (TLRs), which key to generating innate responses infection, may have pathogen-independent roles. We show TLR2 was selectively upregulated by microglia denervated zones hippocampus stereotactic transection axons entorhinal cortex. In mice lacking TLR2, there were transient, selective reductions lesion-induced expression cytokines chemokines. Recruitment T cells, but macrophages, delayed TLR2-deficient mice, as well TNFR1 (tumor necrosis factor receptor 1). deficiency also affected microglial proliferative expansion, whereas all these events unaffected TLR4-mutant mice. Consistent with fact knock-out had returned wild-type levels 8 d, no evidence for effects on neuronal plasticity at 20 d. These results identify role early glial brain injury, acting an bridge neuroinflammation.