The aim of this study was to characterize TLR2-mediated inflammation and correlate Tlr2 gene expression with the volume of ischemic brain lesions in adult mice. Ischemic lesions in Wt(Tlr2-luc) and Tlr2-/-(Tlr2-luc) mice were induced by the tMCAO method. Mice were imaged by MRI and BLI throughout 7 days after tMCAO to longitudinally monitor the progression of the ischemic lesion and the associated inflammation. Imaging results were complemented by neurological deficit assessment, analysis of microglial inflammation markers, and determining cytokine levels in blood plasma. The activity of the Tlr2 gene promoter, monitored by in vivo bioluminescence, proved to be a great model for monitoring inflammation intensity following a brain stroke. TLR2 deficiency caused the formation of a larger ischemic lesion and increased edema; however, survival was not affected. Inflammation reduction was quicker with more prominent neurological recovery. Additionally, the volume of the ischemic lesion positively correlated with the neurological deficit and the inflammation intensity, regardless of TLR2 presence. TLR2 deficiency caused a reduction in inflammatory microglial markers and increased levels of pro-inflammatory and anti-inflammatory cytokines in blood, indicating its dual role. Overall, this research showed that TLR2 deficiency changed the dynamics of inflammatory processes after ischemic brain injury and facilitated neurological recovery in the acute phase of brain ischemia in mice.