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首页> 外文期刊>Neuron >The Glia-Derived Alarmin IL-33 Orchestrates the Immune Response and Promotes Recovery following CNS Injury
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The Glia-Derived Alarmin IL-33 Orchestrates the Immune Response and Promotes Recovery following CNS Injury

机译：胶质细胞衍生的Alarmin IL-33协调免疫反应并促进CNS损伤后的恢复

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摘要

Inflammation is a prominent feature of CNS injury that heavily influences neuronal survival, yet the signals that initiate and control it remain poorly understood. Here we identify the nuclear alarmin, interleukin (IL)-33, as an important regulator of the innate immune response after CNS injury. IL-33 is expressed widely throughout the healthy brain and is concentrated in white mater due to predominant expression in post-mitotic oligodendrocytes. IL-33 is released immediately after CNS injury from damaged oligodendrocytes, acting on local astrocytes and microglia to induce chemokines critical for monocyte recruitment. Mice lacking IL-33 have impaired recovery after CNS injury, which is associated with reduced myeloid cell infiltrates and decreased induction of M2 genes at the injury site. These results demonstrate a novel molecular mediator contributing to immune cell recruitment to the injured CNS and may lead to new therapeutic insights in CNS injury and neurodegenerative diseases.
机译：炎症是中枢神经系统损伤的一个突出特征，它严重影响神经元的存活，但引发和控制神经损伤的信号仍然知之甚少。在这里，我们确定了核警报蛋白白介素（IL）-33，是中枢神经系统损伤后先天免疫反应的重要调节剂。 IL-33在整个健康大脑中广泛表达，并且由于有丝分裂后少突胶质细胞的主要表达而集中在白色物质中。 CNS损伤后，受损的少突胶质细胞会立即释放IL-33，作用于局部星形胶质细胞和小胶质细胞，诱导对​​单核细胞募集至关重要的趋化因子。缺乏IL-33的小鼠在CNS损伤后恢复能力受损，这与髓样细胞浸润减少和损伤部位M2基因的诱导降低有关。这些结果证明了一种新型分子介体，有助于免疫细胞募集至受伤的中枢神经系统，并可能导致中枢神经系统损伤和神经退行性疾病的新治疗方法。

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