The neuroinflammatory mechanisms following ischemic stroke involve intricate interactions across several dimensions: (1) Glial cell activation and polarization post-ischemia: Microglia, the predominant immune cells in brain tissue, recognize damage-associated molecular patterns (DAMPs) through pattern recognition receptors (e.g., Toll-like receptor 4, TLR4), initiating M1 pro-inflammatory polarization and releasing substantial inflammatory mediators. The gene discussed is TLR4; the disease is ischemia.