Premium
Novel therapeutic strategies targeting innate immune responses and early inflammation after stroke
Author(s) -
Shichita Takashi,
Ago Tetsuro,
Kamouchi Masahiro,
Kitazono Takanari,
Yoshimura Akihiko,
Ooboshi Hiroaki
Publication year - 2012
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2012.07941.x
Subject(s) - inflammation , neuroprotection , immune system , immunology , innate immune system , microglia , medicine , neuroinflammation , pharmacology
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 TLR 4 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.