Abstract
Pivotal roles of innate immunity in post-ischemic inflammation have recently attracted attention. The regulation of innate immune responses could be a promising neuroprotective therapy. Damage-associated molecular patterns (DAMPs) which are released from ischemic brain tissue activate infiltrating immune cells via Toll-like receptor 2 (TLR2) and TLR4. IL-23 is produced from activated macrophage and induces IL-17 production from infiltrating γδT cells. This IL-23/IL-17 inflammatory axis mediates ischemic brain injuries in the delayed phase (24 hours after stroke onset). Anti-IL-23 and anti-IL-17 neutralizing antibodies as well as new immunoregulators (e.g. FTY720) could be candidates for new neuroprotective agents which have a long therapeutic time window. Modulation of each process of post-ischemic inflammation would enable us to establish novel neuroprotective strategies for ischemic stroke.
