A robust innate immune activation leads to downstream expression of inflammatory mediators that amplify tissue damage and consequently increase the morbidity after stroke. The Toll-like receptor 4 (TLR4) pathway is a major innate immune pathway activated acutely and chronically after stroke. Hence, understanding the intricacies of the temporal profile, specific control points, and cellular specificity of TLR4 activation is crucial for the development of any novel therapeutics targeting the endogenous innate immune response after focal cerebral ischemia. The goal of this review is to summarize the current findings related to TLR4 signaling after stroke with a specific focus on the components of the neurovascular unit such as astrocytes, neurons, endothelial cells, and pericytes. In addition, this review will examine the effects of focal cerebral ischemia on interaction of these neurovascular unit components.
Keywords: Focal cerebral ischemia; Innate immunity; Neurovascular unit; TLR4; Toll-like receptor.