Ischemic stroke initiates a robust inflammatory response that starts in the intravascular
compartment and involves rapid activation of brain resident cells. A key mechanism of this
inflammatory response is the migration of circulating immune cells to the ischemic brain
facilitated by chemokine release and increased endothelial adhesion molecule expression.
Brain-invading leukocytes are well-known contributing to early-stage secondary ischemic
injury, but their significance for the termination of inflammation and later brain repair has …