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首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Low and dysregulated production of follistatin in immune cells of relapsing-remitting multiple sclerosis patients.
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Low and dysregulated production of follistatin in immune cells of relapsing-remitting multiple sclerosis patients.

机译：复发缓解型多发性硬化症患者免疫细胞中卵泡抑素的产量低且失调。

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One of the mechanisms known to play a key role in neuronal and oligodendroglial fate specification of neural stem cells (NSCs) is restriction of bone morphogenic proteins (BMP) signaling by BMP antagonists. Here, we demonstrate that follistatin mRNA and protein secreted levels in peripheral blood mononuclear cells (PBMCs) of relapsing-remitting multiple sclerosis (RR-MS) patients are significantly reduced compared to healthy controls (HC). We also observed a different profile of regulation mechanisms. Follistatin was similarly expressed and secreted by T lymphocytes and monocytes among the PBMCs of HC, and follistatin upregulation of HC was subjected to stimulation with both LPS and TNF-alpha. Among PBMCs of RR-MS patients, however, follistatin was found to be downregulated in their monocytes and unresponsive to stimulation with either LPS or TNF-alpha. Our results may shed some light on the mechanisms involved in remyelination failure in MS, which may be related to the inability of RR-MS patients' immune cells to provide a sufficient pro-neurogenic and oligodendrogenic niche, by expressing and secreting follistatin, in addition to the previously described noggin reduced expression. Our results indicate that the low expression of follistatin in immune cells of patients with RR-MS is a result of the altered immunoregulation of monocytes in these patients.
机译：已知在神经干细胞（NSCs）的神经元和少突神经胶质命运规范中发挥关键作用的机制之一是BMP拮抗剂对骨形态发生蛋白（BMP）信号传导的限制。在这里，我们证明复发缓解型多发性硬化症（RR-MS）患者的外周血单个核细胞（PBMC）中的卵泡抑素mRNA和蛋白分泌水平与健康对照（HC）相比显着降低。我们还观察到了不同的调节机制。卵泡抑素在HC的PBMC中也由T淋巴细胞和单核细胞类似地表达和分泌，并且LPS和TNF-α都刺激了HC的卵泡抑素上调。然而，在RR-MS患者的PBMC中，发现卵泡抑素在其单核细胞中被下调，并且对LPS或TNF-α刺激均无反应。我们的研究结果可能揭示了MS髓鞘再生失败的机制，这可能与RR-MS患者的免疫细胞无法通过表达和分泌卵泡抑素来提供足够的促神经原性和少突胶质生成的利基有关。与先前描述的头蛋白还原表达有关。我们的结果表明，RR-MS患者免疫细胞中卵泡抑素的低表达是这些患者单核细胞免疫调节改变的结果。

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