TLR4 signal ablation attenuated neurological deficits by regulating microglial M1/M2 phenotype after traumatic brain injury in mice

Traumatic brain injury (TBI) initiates inflammatory responses that result in an enduring cascade of secondary neuronal loss and behavioural impairment. Toll-like receptor 4 (TLR4), predominantly expressed by microglia, recognizes damage-associated molecular patterns (DAMPs) and regulates inflammatory processes. Interestingly, the switch of microglial M1/M2 phenotypes after TBI is highly important regarding damage and restoration of neurological function. Therefore, we investigated the role and mechanisms of the TLR4 signalling pathway in regulating microglial M1/M2 phenotypes. (Source: Journal of Neuroimmunology)

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