Novel therapeutic strategies targeting innate immune responses and early inflammation after stroke

Takashi Shichita, Tetsuro Ago, Masahiro Kamouchi, Takanari Kitazono, Akihiko Yoshimura, Hiroaki Ooboshi

Research output: Contribution to journalArticle

97 Citations (Scopus)


Post-ischemic inflammation is an essential step in the progression of ischemic stroke. This review focuses on the function of infiltrating immune cells, macrophages, and T cells, in ischemic brain injury. The brain is a sterile organ; however, the activation of Toll-like receptor (TLR) 2 and TLR4 is pivotal in the beginning of post-ischemic inflammation. Some endogenous TLR ligands are released from injured brain cells, including high mobility group box 1 and peroxiredoxin family proteins, and activate the infiltrating macrophages and induce the expression of inflammatory cytokines. Following this step, T cells also infiltrate into the ischemic brain and mediate post-ischemic inflammation in the delayed phase. Various cytokines from helper T cells and γδT cells function as neurotoxic (IL-23/IL-17, IFN- γ) or neuroprotective (IL-10, IL-4) mediators. Novel neuroprotective strategies should therefore be developed through more detailed understanding of this process and the regulation of post-ischemic inflammation.

Original languageEnglish
Pages (from-to)29-38
Number of pages10
JournalJournal of Neurochemistry
Issue numberSUPPL. 2
Publication statusPublished - 2012 Nov



  • cytokine
  • DAMPs
  • macrophage
  • Tcell
  • TLR

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

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