title: [Post-ischemic innate immunity and its application for novel therapeutic strategy targeting brain inflammation].
abstract: Stroke or brain ischemia is one of the major causes of death and disability worldwide. Post-ischemic inflammation is an essential step in the progression of brain ischemia-reperfusion injury. In a mouse stroke model, we have reported that IL-23 produced from infiltrating macrophages induces IL-17 producing T cells. IL-17 is mainly produced from gammadeltaT cells and promotes delayed (day 3-4) ischemic brain damage. We also demonstrated that peroxiredoxin (Prx) family proteins released extracellularly from necrotic brain cells induce expression of inflammatory cytokines including IL-23 in macrophages through activation of Toll-like receptor 2(TLR2) and TLR4, thereby promoting neural cell death. We thus propose that regulation of the IL-23-IL-17 axis including gammadeltaT cells, macrophages, and extracellular Prxs could be a potent neuroprotective tool.
authors: Department of Microbiology and Immunology, Keio University School of Medicine.
authors: Minako
authors: M
authors: Ito
authors: Taisuke
authors: T
authors: Kondo
authors: Takashi
authors: T
authors: Shichita
authors: Akihiko
authors: A
authors: Yoshimura
mesh_terms: D000818:Animals; D002545:Brain Ischemia / Q000276:immunology / Q000378:metabolism / Q000517:prevention & control / Q000628:therapy*; D004195:Disease Models, Animal; D004660:Encephalitis / Q000150:complications / Q000276:immunology / Q000378:metabolism / Q000628:therapy*; D006801:Humans; D007113:Immunity, Innate / Q000276:immunology*; D007378:Interleukins / Q000276:immunology / Q000378:metabolism
chemical_list: D007378:Interleukins