J Autoimmunity:ETS-1通过上调CIRBP促进炎症性肠病中Th1细胞介导的黏膜炎症

2022-08-14 MedSci原创 MedSci原创

该研究数据表明ETS-1在炎症性肠病(IBD)患者中高度表达,并通过冷诱导RNA结合蛋白(CIRBP)促进Th1驱动的粘膜炎症。CIRBP可作为治疗人类IBD的新治疗靶点。

目的作为人类炎症性肠病(IBD)的易感基因,禽成红细胞增多症病毒E26癌基因同源物1 (ETS-1)如何调节肠黏膜免疫反应仍不清楚。在这篇研究中探索了ETS-1IBD发病机制中的潜在作用。

方法IBD患者中检查ETS-1表达。构建了CD45RBhighCD4+ T细胞转移结肠炎、葡聚糖硫酸钠(DSS)诱导的结肠炎和偶氮甲烷(AOM/DSS诱导的结肠炎相关癌(CAC)模型,以探讨ETS-1在体内的功能。对来自Ets-1转基因(Tg)小鼠的CD4+ T细胞进行 RNA测序,以破译关键的差异表达基因。进行腺病毒转导以验证ETS-1在体内的治疗潜力。

结果与健康对照相比,来自活动性IBD患者的CD4+ T细胞中ETS-1表达显著增加,其被TNF-α上调,但被抗TNF-α单克隆抗体治疗显著抑制。与对照组相比,在用Ets-1TgCD45RBhighCD4+ T细胞重建的Rag1-/-小鼠或在DSS暴露后的Ets-1 Tg小鼠中观察到更严重的结肠炎,其特征是炎症结肠中TNF-α和IFN-γ的表达更高。Ets-1 Tg小鼠更容易发生AOM/DSS诱导的CAC,骨髓嵌合体进一步证明固有层免疫细胞而非肠上皮细胞促成了结肠炎的发生。RNA测序和荧光素酶分析显示冷诱导RNA结合蛋白(CIRBP)作为ETS-1 的功能靶标,可促进Th1细胞驱动的免疫反应。一致地,腺病毒-m-cirbp-shRNA的腹腔内给药改善了三硝基苯磺酸(TNBS)诱导的Ets-1 Tg小鼠结肠炎。

结论该研究数据表明ETS-1IBD患者中高度表达,并通过CIRBP促进Th1驱动的粘膜炎症。CIRBP可作为治疗人类IBD的新治疗靶点。

 

出处:He Q, Gao H, Chang YL, Wu X, Lin R, Li G, Lin J, Lu H, Chen H, Li Z, Cong Y, Yao J, Liu Z. ETS-1 facilitates Th1 cell-mediated mucosal inflammation in inflammatory bowel diseases through upregulating CIRBP. J Autoimmun. 2022 Aug 1;132:102872. doi: 10.1016/j.jaut.2022.102872. Epub ahead of print. PMID: 35926374.

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    2022-08-25 ms7000000017147997

    学习到了

    0

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    2022-08-15 snowpeakxu
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