| 孔庆飞,张晓莉,朱 伟,王丹丹,曲思盈,崔英哲,敬 佳,穆莉莉,李呼伦.IRF5调控AChR特异性T细胞参与EAMG疾病发生、发展的实验研究[J].,2018,(1):27-31 |
| IRF5调控AChR特异性T细胞参与EAMG疾病发生、发展的实验研究 |
| IRF5 was involved in the Occurrence and Development of EAMG via Regulating AChR-specific T cells |
| 投稿时间：2017-06-11 修订日期：2017-06-30 |
| DOI：10.13241/j.cnki.pmb.2018.01.006 |
| 中文关键词: 重症肌无力 干扰素调节因子5 实验性自身免疫性重症肌无力 乙酰胆碱受体 |
| 英文关键词: Myasthenia Gravis Interferon regulatory factor 5 Experimental Autoimmune Myasthenia Gravis Acetylcholine Receptor |
| 基金项目:黑龙江省教育厅科学技术研究重点项目（12541z008） |
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| 中文摘要: |
| 摘要 目的：体内外实验探讨干扰素调节因子5（Interferon regulatory factor 5, IRF5）在乙酰胆碱受体（Acetylcholine Receptor，AChR）特异性T、B细胞中的表达情况以及与实验性自身免疫性重症肌无力（Experimental Autoimmune Myasthenia Gravis, EAMG）疾病的发生存在的可能关系。方法：ELISA法检测不同发病时相大鼠血清中IRF5的含量；流式细胞仪法检测早期晚期发病时相CD4+T 细胞以及CD45R+B细胞中IRF5的表达情况；QPCR法及Western blotting法分别检测体外AChR刺激不同时间点的T、B细胞中IRF5的mRNA和蛋白水平的表达差异。结果：血清学检测结果显示，IRF5高表达于EAMG大鼠的晚期发病时相的血清中，并随着疾病进程的不断加重呈现逐渐增高的表达，与CFA对照组大鼠相比较差异显著，有统计学意义（***，P< 0.001）；流式结果表明，来自EAMG大鼠早、晚期发病时相的无论是淋巴结还是脾脏中的AChR特异性T细胞均高表达IRF5，且与CFA对照组相比较，有统计学差异，而B细胞中IRF5的表达即便是在晚期发病时相也与CFA对照组无明显区别；QPCR结果发现，EAMG晚期发病时相的AChR特异性T细胞在经过AChR体外刺激0 h，72 h后，均可见IRF5 mRNA水平的高表达，而B细胞中IRF5的mRNA水平则在两组中无统计学差异；Western blotting结果进一步证实，IRF5蛋白水平在AChR特异性T细胞中呈现高表达。结论：IRF5是通过对AChR特异性T淋巴细胞的调控进而参与EAMG疾病的发生和发展过程的。 |
| 英文摘要: |
| ABSTRACT Objective: To explore the expression of IRF5 on AChR-specific T and B cells, as well as the potential relationship be- tween IRF5 and EAMG occurrence via both in vivo and in vitro tests. Methods: The contents of IRF5 in serum at different phases of dis- ease were detected by ELISA. The expression of IRF5 on CD4+T cells and CD45R+B cells at both early and late phases of this disease was measured by flow cytometry. QPCR and western blotting were selected to evaluate IRF5 mRNA and protein expression levels on AChR-specific T and B cells after different time of AChR incubation. Results: Compared with CFA group, IRF5 highly expressed in the serum of the late phase of EAMG rats, and IRF5 in serum presented a gradual increase in expression increased with the severer process of EAMG disease, (***, P<0.001). Flow data showed that, AChR-specific T cells from lymph nodes and spleen expressed higher levels of IRF5 compared with that of CFA group (**, P<0.01, ***, P<0.001), while no significance of IRF5 expression between AChR-specific B cells and non-specific B cells from CFA rats. QPCR results replied that AChR-specific T cells from late phase of EAMG disease had more IRF5 mRNA expression with 0 h and 72 h AChR in vitro incubation, while no difference was found in AChR-specific B cells, com- pared with cells from CFA rats. What's more, we also detected more IRF5 protein expression levels in AChR stimulated T cells. Conclusion: IRF5 was involved in the occurrence and development of EAMG via regulating AChR-specific T cells. |
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