[Post-ischemic innate immunity and its application for novel therapeutic strategy targeting brain inflammation].

Minako Ito, Taisuke Kondo, Takashi Shichita, Akihiko Yoshimura

Research output: Contribution to journalArticle

3 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)1291-1301
Number of pages11
JournalNihon rinsho. Japanese journal of clinical medicine
Volume71
Issue number7
Publication statusPublished - 2013 Jul

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Interleukin-23
Interleukin-17
Encephalitis
Innate Immunity
Brain Ischemia
Stroke
Macrophages
Peroxiredoxins
Toll-Like Receptor 2
Macrophage Activation
Brain
Reperfusion Injury
Cause of Death
Cell Death
Therapeutics
Cytokines
Inflammation
T-Lymphocytes
Proteins

ASJC Scopus subject areas

  • Medicine(all)

Cite this

[Post-ischemic innate immunity and its application for novel therapeutic strategy targeting brain inflammation]. / Ito, Minako; Kondo, Taisuke; Shichita, Takashi; Yoshimura, Akihiko.

In: Nihon rinsho. Japanese journal of clinical medicine, Vol. 71, No. 7, 07.2013, p. 1291-1301.

Research output: Contribution to journalArticle

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