Targeting inflammation-immune response as a novel strategy for the treatment of brain infarction

中风后的免疫反应仍然是一个活跃的研究领域。先前的研究表明，淋巴细胞会导致预后恶化。然而，T淋巴细胞亚群的作用尚未得到很好的研究。我们最近报道，在巨噬细胞来源的IL-23的刺激下，γ-DeltaT细胞可以产生IL-17。这些细胞因子似乎对中风的进化有负面影响，因为缺乏这些细胞因子的小鼠受到了保护。在这项研究中，过氧化还蛋白(PRX)，一种内源性抗氧化剂，被确定为危险信号。研究表明，Prx通过Toll样受体-2和-4途径诱导IL-23并导致卒中预后恶化。这些发现表明，PRX是一种新的损伤相关分子模式(DAMPS)，抑制PRX似乎具有保护作用。

Immune responses following stroke continue to be an active area of investigation. Prior work has shown that lymphocytes lead to worsened outcome. However, the role of T lymphocyte subtypes has not been well studied. We have recently reported that the gamma-deltaT cells can produce IL-17 following stimulation by macrophage derived IL-23. These cytokines appear to contribute negatively to stroke evolution, as mice deficient in these cytokines are protected. In this study, peroxiredoxin (Prx), an endogenous antioxidant, was identified as a danger signal. Prx is shown to induce IL-23 and leads to worsened stroke outcome through toll-like receptors-2 and -4 pathway. These findings show that Prx is a novel damage-associated molecular patterns (DAMPs) and inhibiting Prx appears to be protective.