Post-ischemic inflammation in the brain.
Post-ischemic inflammation in the brain.
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DOI：
10.3389/fimmu.2012.00132
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发表时间：
2012
影响因子：
7.3
通讯作者：
Yoshimura A
中科院分区：
文献类型：
--
作者：
Shichita T;Sakaguchi R;Suzuki M;Yoshimura A
缺血后炎症是脑缺血再灌注损伤进展的重要步骤。在这篇综述中，我们重点关注浸润性免疫细胞、巨噬细胞和 T 淋巴细胞引发的缺血后炎症。脑缺血是一个无菌器官，但损伤引起的炎症主要依赖于Toll样受体（TLR）2和TLR4。特别是一些内源性 TLR 配体、高迁移率族蛋白 1 (HMGB1) 和过氧化还原蛋白家族蛋白，与浸润巨噬细胞的激活和炎症细胞因子表达有关。巨噬细胞激活后，T 淋巴细胞浸润缺血脑并调节延迟期炎症。巨噬细胞产生的 IL-23 诱导产生 IL-17 的 γδT 淋巴细胞促进缺血性脑损伤，而调节性 T 淋巴细胞则抑制炎症介质的功能。对浸润免疫细胞炎症机制的更深入了解可能会导致新型神经保护疗法的开发。
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 and TLR4. Some endogenous TLR 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. IL-17-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.