Journal
JOURNAL OF NEUROCHEMISTRY
Volume 123, Issue -, Pages 29-38Publisher
WILEY
DOI: 10.1111/j.1471-4159.2012.07941.x
Keywords
cytokine; DAMPs; macrophage; T cell; TLR
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Funding
- Ministry of Education, Culture, Sports, Science and Technology of Japan [S0801084, 23591262]
- PRESTO from Japan Science and Technology Agency
- CREST from Japan Science and Technology Agency
- Grants-in-Aid for Scientific Research [23591262] Funding Source: KAKEN
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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 ?dT cells function as neurotoxic (IL-23/IL-17, IFN-?) 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.
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