CCL2 and Stroke: Another mechanism mediating the accumulation of myeloid cells in the brain is the release of chemokines such as CCL2 (MCP1) and CCL3 (MIP1α), which function as chemoattractant factors amplifying cell recruitment in brain injury, including stroke and cerebral hypoperfusion.55, –57 We found that CCL2 and CCL3 expression was increased in the vasculature duing hypoperfusion, and significantly reduced by Nox2 KO following carotid stenosis.