Temporal analysis with flow cytometry of the microglial/macrophage activation profiles in TLR2-KO mice and age-matched controls revealed reduced microglial/macrophage activation after stroke and reduced capacity of resident microglia to proliferate, as well as decreased levels of monocyte chemotactic protein-1 (MCP-1) and consequently lower levels of CD45 high/CD11b+ expressing cells [61]. The gene discussed is CCL2; the disease is stroke disorder.