Abstract
Inflammation is an essential step in the progression of ischemic stroke pathology. Various mechanisms of innate immunity are implicated in the acute sterile inflammation following ischemic brain injury. Ischemic insults induce the necrotic death of brain cells, which leads to the extracellular release of danger-associated molecular patterns (DAMPs). DAMPs are recognised by pattern recognition receptors (PRRs) in innate immune cells. IL-1β and various neurotoxic mediators are produced by the activation of PRRs. Caspase-1 activation and the formation of inflammasome complex are essential for the production of the active form of IL-1β in ischemic stroke. Recent evidence has supported the use of new therapeutic opportunities for ischemic stroke by targeting DAMPs and inflammasome. This review examines the evidence regarding the essential roles of innate immunity in the creation of novel treatments for ischemic stroke.
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Shichita, T., Ito, M., Morita, R., Yoshimura, A. (2016). The Role of Innate Immunity in Ischemic Stroke. In: Miyasaka, M., Takatsu, K. (eds) Chronic Inflammation. Springer, Tokyo. https://doi.org/10.1007/978-4-431-56068-5_49
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DOI: https://doi.org/10.1007/978-4-431-56068-5_49
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