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首页> 外文期刊>Clinical and Experimental Immunology: An Official Journal of the British Society for Immunology >Neuroprotection effect of interleukin (IL)-17 secreted by reactive astrocytes is emerged from a high-level IL-17-containing environment during acute neuroinflammation
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Neuroprotection effect of interleukin (IL)-17 secreted by reactive astrocytes is emerged from a high-level IL-17-containing environment during acute neuroinflammation

机译：反应性星形胶质细胞分泌的白介素（IL）-17的神经保护作用是在急性神经发炎期间从高水平的含IL-17的环境中产生的

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An increase in interleukin (IL)-17A-producing cells, particularly at sites of tissue inflammation, is observed frequently, yet the mechanism is not fully understood. This study aims to dissect the role of IL-17 in autoimmunity-mediated neuroinflammation. The cytokine milieu containing elevated IL-17, which often appears in active states of autoimmunity, was mimicked in vitro by a supernatant obtained from rat peripheral blood monocytes stimulated with phorbol mystistate acetate (PMA)/ionomycin. The application of such inflammatory media on only primary cultured cerebellar granule neurones resulted in significant apoptosis, but the presence of astrocytes largely prevented the effect. The supernatants of the stimulated astrocytes, especially those that contained the highest level of IL-17, achieved the best protection, and this effect could be blocked by anti-IL-17 antibodies. Protein IL-17 inhibited intracellular calcium increase and protected the neurones under inflammatory attack from apoptosis. IL-17, but not interferon (IFN)-γ, in the inflammatory media contributed to astrocyte secretion of IL-17, which depended on the Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway activation. The astrocytes that were treated with IL-17 alone or with prolonged treatment of the inflammatory media failed to produce sufficient levels of IL-17. Moreover, confirmatory data were obtained in vivo in a monophasic experimental autoimmune uveitis (EAU) in Lewis rats; in this preparation, the high-level IL-17-containing the cytokine milieu was demonstrated, along with IL-17 secretion by the resident neural cells. The antagonism of IL-17 at a late stage disturbed the disease resolution and resulted in significant neural apoptosis. Our data show a dynamic role of IL-17 in the maintenance of homeostasis and neuroprotection in active neuroinflammation.
机译：经常观察到产生白介素（IL）-17A的细胞增多，特别是在组织炎症部位，但这种机理尚未完全明了。这项研究旨在剖析IL-17在自身免疫介导的神经炎症中的作用。在体外，通过从受佛波乙酸Mystat状态的乙酸（PMA）/离子霉素刺激的大鼠外周血单核细胞获得的上清液，可以模拟出常以自身免疫活性状态出现的，含有升高的IL-17的细胞因子环境。仅在原代培养的小脑颗粒神经元上使用这种炎症介质会导致明显的细胞凋亡，但星形胶质细胞的存在很大程度上阻止了这种作用。受刺激的星形胶质细胞的上清液，特别是那些含有最高水平的IL-17的上清液，具有最佳的保护作用，这种作用可以被抗IL-17抗体阻断。 IL-17蛋白可抑制细胞内钙的增加，并保护炎症反应中的神经元免于凋亡。炎性介质中的IL-17而不是干扰素（IFN）-γ有助于星形胶质细胞分泌IL-17，这取决于Janus激酶/信号转导子和转录激活子（JAK / STAT）途径的激活。单独用IL-17或长期治疗炎性介质治疗的星形胶质细胞不能产生足够水平的IL-17。此外，在Lewis大鼠单相实验性自身免疫性葡萄膜炎（EAU）中体内获得了证实性数据;在该制剂中，证实了含有高水平IL-17的细胞因子环境，以及驻留神经细胞分泌的IL-17。 IL-17在后期的拮抗作用干扰了疾病的解决，并导致了明显的神经细胞凋亡。我们的数据显示IL-17在活动性神经炎症中维持体内稳态和神经保护的动态作用。

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