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首页> 美国卫生研究院文献>Scientific Reports >In patients with chronic aplastic anemia bone marrow–derived MSCs regulate the Treg/Th17 balance by influencing the Notch/RBP-J/FOXP3/RORγt pathway
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In patients with chronic aplastic anemia bone marrow–derived MSCs regulate the Treg/Th17 balance by influencing the Notch/RBP-J/FOXP3/RORγt pathway

机译：在慢性再生障碍性贫血患者中骨髓间充质干细胞通过影响Notch / RBP-J / FOXP3 /RORγt途径来调节Treg / Th17平衡

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The standard treatment for aplastic anemia (AA) in young patients is a matched sibling hematopoietic stem cell transplant. Transfusion of a chronic AA patient with allogeneic bone marrow–derived mesenchymal stromal cells (BMMSCs) is currently being developed as a cell-based therapy, and the safety and efficacy of such transfusions are being continuously improved. Nevertheless, the mechanisms by which BMMSCs exert their therapeutic effects remain to be elucidated. In this study, mesenchymal stromal cells (MSCs) obtained from bone marrow donors were concentrated and intravenously injected into 15 chronic AA patients who had been refractory to prior immunosuppressive therapy. We showed that BMMSCs modulate the levels of Th1, Th2, Th17 and Treg cells, as well as their related cytokines in chronic AA patients. Furthermore, the percentages of Th1 and Th17 cells among the H-MSCs decreased significantly, while the percentage Treg cells increased. The Notch/RBP-J/FOXP3/RORγt pathway was involved in modulating the Treg/Th17 balance after MSCs were transfused in vitro. Additionally, the role played by transfused MSCs in regulating the Treg/Th17 balance via the Notch/RBP-J/FOXP3/RORγt pathway was further confirmed in an AA mouse model. In summary, in humans with chronic AA, BMMSCs regulate the Treg/Th17 balance by affecting the Notch/RBP-J/FOXP3/RORγt pathway.
机译：青年患者再生障碍性贫血（AA）的标准治疗方法是匹配的同胞造血干细胞移植。目前正在开发一种慢性AA患者同种异体骨髓源性间充质基质细胞（BMMSCs）的输血，作为一种基于细胞的疗法，这种输血的安全性和有效性正在不断提高。然而，BMMSC发挥其治疗作用的机制仍有待阐明。在这项研究中，将从骨髓供体获得的间充质基质细胞（MSC）浓缩并静脉注射到15例先前对免疫抑制治疗无效的慢性AA患者中。我们表明，BMMSCs在慢性AA患者中调节Th1，Th2，Th17和Treg细胞的水平及其相关的细胞因子。此外，H-MSC中Th1和Th17细胞的百分比显着下降，而Treg细胞的百分比则上升。 MSCs体外输注后，Notch / RBP-J / FOXP3 /RORγt通路参与调节Treg / Th17平衡。另外，在AA小鼠模型中进一步证实了输注的MSC通过Notch / RBP-J / FOXP3 /RORγt途径调节Treg / Th17平衡的作用。总之，在患有慢性AA的人中，BMMSC通过影响Notch / RBP-J / FOXP3 /RORγt途径来调节Treg / Th17平衡。

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