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

Abstract:

: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.

journal_name

J Neurochem

authors

Shichita T,Ago T,Kamouchi M,Kitazono T,Yoshimura A,Ooboshi H

doi

10.1111/j.1471-4159.2012.07941.x

subject

Has Abstract

pub_date

2012-11-01 00:00:00

pages

29-38

eissn

0022-3042

issn

1471-4159

journal_volume

123 Suppl 2

pub_type

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