title: [DAMPs (damage-associated molecular patterns) and inflammation].
abstract: Post-ischemic inflammation is re-appraised as an important player in the progression of ischemic stroke. Activation of inflammatory cells via Toll-like receptor 2 (TLR2) and TLR4 is caused by several damage-associated molecular patterns (DAMPs), including high mobility group box-1 (HMGB-1) and heat shock proteins. We have recently found that peroxiredoxin (Prx) is one of the strong DAMPs and activates infiltrating macrophages in brain ischemia. We have also found that interleukin-23 (IL-23) from the activated macrophages stimulates γδT cells which release IL-17, thereby causing the delayed expansion of infarct lesions. Further investigation of the innate immune response would lead to development of novel stroke treatment with a broad therapeutic time window.
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Ooboshi
authors.forename: Takashi
authors.initials: T
authors.lastname: Shichita
mesh_terms: D001921:Brain / Q000473:pathology; D018450:Disease Progression; D024243:HMGB1 Protein; D006360:Heat-Shock Proteins; D006801:Humans; D007113:Immunity, Innate; D007249:Inflammation / Q000235:genetics* / Q000276:immunology; D020381:Interleukin-17; D053759:Interleukin-23; D008262:Macrophage Activation; D054464:Peroxiredoxins / Q000502:physiology; D020521:Stroke / Q000235:genetics / Q000276:immunology; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4
chemical_list: D024243:HMGB1 Protein; C585491:HMGB1 protein, human; D006360:Heat-Shock Proteins; D020381:Interleukin-17; D053759:Interleukin-23; C495342:TLR2 protein, human; C495345:TLR4 protein, human; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4; D054464:Peroxiredoxins