Post-ischemic inflammation in the brain

Takashi Shichita, Ryota Sakaguchi, Mayu Suzuki, Akihiko Yoshimura

Research output: Contribution to journalReview article

116 Citations (Scopus)

Abstract

Post-ischemic inflammation is an essential step in the progression of brain ischemia-reperfusion injury. In this review, we focus on the post-ischemic inflammation triggered by infiltrating immune cells, macrophages, and T lymphocytes. Brain ischemia is a sterile organ, but injury-induced inflammation is mostly dependent on Toll-like receptor (TLR) 2 andTLR4. Some endogenousTLR ligands, high mobility group box 1 (HMGB1) and peroxiredoxin family proteins, in particular, are implicated in the activation and inflammatory cytokine expression in infiltrating macrophages. Following macrophage activation, T lymphocytes infiltrate the ischemic brain and regulate the delayed phase inflammation. IL17-producing γδT lymphocytes induced by IL-23 from macrophages promote ischemic brain injury, whereas regulatory T lymphocytes suppress the function of inflammatory mediators. A deeper understanding of the inflammatory mechanisms of infiltrating immune cells may lead to the development of novel neuroprotective therapies.

Original languageEnglish
Article numberArticle 132
JournalFrontiers in Immunology
Volume3
Issue numberMAY
DOIs
Publication statusPublished - 2012 Dec 1

Keywords

  • Brain
  • Cytokine
  • Damps
  • Inflammation
  • Ischemia
  • Macrophages
  • Stroke,T cells

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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