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Roles for innate immunity in neurological and psychiatric disorders

開催日 2014/9/12
時間 17:10 - 19:10
会場 Room E(301)
Chairperson(s) 山中 宏二 / Koji Yamanaka (名古屋大学環境医学研究所病態神経科学分野 / Research Institute of Environmental Medicine, Nagoya University, Japan)
古屋敷 智之 / Tomoyuki Furuyashiki (神戸大学大学院医学研究科薬理学 / Division of Pharmacology, Kobe University Graduate School of Medicine, Japan)

Regulation of post-ischemic inflammation by DAMPs and immune cells

  • S2-E-3-2
  • 七田 崇 / Takashi Shichita:1,2 吉村 昭彦 / Akihiko Yoshimura:1 
  • 1:慶應義塾大学医学部 微生物学免疫学教室 / Department of Microbiology and Immunology, School of Medicine, Keio University, Japan 2:科学技術振興機構さきがけ / Precursory Research for Embryonic Science and Technology (PRESTO), Japan Science and Technology Agency, Japan 

Inflammation is an essential step for the pathology of ischemic stroke. Because brain is a sterile organ, the inflammation is triggered by some endogenous molecules which are released from necrotic brain cells. High mobility group box 1 (HMGB1) and peroxiredoxin (Prx) have been recently identified as danger associated molecular patterns (DAMPs) in the ischemic brain. HMGB1 exaggerates the disruption of blood brain barrier in the hyperacute phase; on the other hand, Prx activates infiltrating immune cells and induces the inflammatory cytokine production through TLR2 and TLR4 signaling pathway. Prx family proteins have a common structure for the activation of TLR2 and TLR4. The suppression of this activity by antibody reveals neuroprotective effect in the murine model of transient cerebral ischemia.
Both the extracellular release of Prx and the infiltration of immune cells reach the peak within 1 to 3 days after the onset of ischemic stroke and thereafter they decrease. This will lead to the resolution of post-ischemic inflammation. Indeed, the gene expression profile of infiltrating immune cells in the late phase shows the phenotype for anti-inflammation and tissue repair. The novel neuroprotective strategy for ischemic stroke can be developed by clarifying the detailed mechanisms to turn off the inflammatory response.

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