lncRNA RP11通过PI3K/mTOR信号通路调控抗原提呈B细胞活化

刘明媛; 韩昌鹏; 王珂; 杨月嫦; 单莉莉; 李梦婷; 柯佳; 吴洋; 郭淑芬; 张颖; 韩燕

doi:10.16306/j.1008-861x.2022.03.006

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lncRNA RP11通过PI3K/mTOR信号通路调控抗原提呈B细胞活化

学科前沿 | 更新时间：2022-08-29

- lncRNA RP11通过PI3K/mTOR信号通路调控抗原提呈B细胞活化
- Regulation on activation of antigen presenting B cells with LncRNA RP11 through PI3K/mTOR signaling pathway
- 上海中医药大学学报 2022年36卷第3期页码：30-36
- 作者机构：
  
  1.上海中医药大学附属岳阳中西医结合医院神经内科（上海　200437）
- 作者简介：
  
  刘明媛，女，博士，副主任医师，副教授，主要从事神经免疫和脑血管疾病研究
  韩燕，主任医师，博士生导师；E-mail：hanyan.2006@aliyun.com
- 基金信息：
  
  国家自然科学基金资助项目(81771303)
- DOI：10.16306/j.1008-861x.2022.03.006
  中图分类号：
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刘明媛,韩昌鹏,王珂等.lncRNA RP11通过PI3K/mTOR信号通路调控抗原提呈B细胞活化[J].上海中医药大学学报,2022,36(03):30-36.

LIU Mingyuan,HAN Changpeng,WANG Ke,et al.Regulation on activation of antigen presenting B cells with LncRNA RP11 through PI3K/mTOR signaling pathway[J].Academic Journal of Shanghai University of Traditional Chinese Medicine,2022,36(03):30-36.
刘明媛,韩昌鹏,王珂等.lncRNA RP11通过PI3K/mTOR信号通路调控抗原提呈B细胞活化[J].上海中医药大学学报,2022,36(03):30-36. DOI： 10.16306/j.1008-861x.2022.03.006.

LIU Mingyuan,HAN Changpeng,WANG Ke,et al.Regulation on activation of antigen presenting B cells with LncRNA RP11 through PI3K/mTOR signaling pathway[J].Academic Journal of Shanghai University of Traditional Chinese Medicine,2022,36(03):30-36. DOI： 10.16306/j.1008-861x.2022.03.006.

摘要

目的,2,探索抗原提呈B细胞（APBCs）增殖、活化机制。,方法,2,本研究利用流式分选，获得CD20,+,CD80,+,CD86,+,阳性APBCs细胞，构建lncRNA RP11低表达（KD）和高表达（OE）细胞，并结合体内实验，研究lncRNA RP11对B细胞活化的调控及分子机制。,结果,2,APBCs细胞活化后lncRNA RP11表达显著升高（,P,<,0.01）。lncRNA RP11低表达可显著抑制APBCs的活化，抑制B细胞分泌IgG和IgM（,P,<,0.05，,P,<,0.01）；而在lncRNA RP11高表达细胞中，活化APBCs细胞数量增加，促进细胞分泌IgG和IgM（,P,<,0.05，,P,<,0.01）。同时，在lncRNA RP11高表达细胞中，PI3K/Akt/mTOR通路被激活，而在lncRNA RP11低表达细胞中，该通路活性被明显抑制。mTOR抑制剂的结果表明PI3K/Akt/mTOR信号通路的抑制能降低B细胞的活性水平。在视神经脊髓炎谱系疾病（NMOSD）建模的基础上，使用mTOR激活剂（MHY485）激活mTOR信号通路，小鼠的炎症反应增加，APBCs活化程度也显著升高。,结论,2,lncRNA RP11可以通过调控PI3K/Akt/mTOR通路最终影响B细胞活性。

Abstract

Objective： To explore the mechanism of antigen-presenting B cells （APBCs） proliferationand activation.,Methods,2,In this study， flow cytometric sorting was used to filter the CD20,+,CD80,+,CD86,+, positive APBCs. lncRNA RP11 knock-down （KD） and over-expressed （OE） cells were constructed， and combined with ,in vivo, experiments， the regulation and molecule mechanism of lncRNA RP11 on APBCs activation was investigated.,Results,2,The expression of lncRNA RP11 was increased significantly after APBCs activation. Low expression of lncRNA RP11 could significantly inhibit the activation of APBCs and secretion of IgG and IgM by B cells. While the number of activated APBCs was significantly increased and secretion of IgG and IgM was promoted in over-expressed lncRNA RP11 cells. At the same time， PI3K/Akt/mTOR pathway was activated in over-expressed lncRNA RP11 cells， but the pathway was significantly inhibited in knock-down lncRNA RP11 cells. The results of mTOR inhibitors tests confirmed that the activity level of APBCs was down-regulated because of the inhibition of the PI3K/Akt/mTOR pathway. On the basis of neuromyelitis optica spectrum disease （NMOSD） modeling， mTOR activator （MHY485） was used to activate mTOR signaling pathway， the mice inflammatory response increased and the activation degree of APBCs significantly promoted.,Conclusion,2,LncRNA RP11 can influence B cell activity by regulating PI3K/Akt/mTOR pathway.

关键词

抗原提呈B细胞lncRNA RP11PI3K/Akt/mTOR通路视神经脊髓炎谱系疾病

Keywords

antigen-presenting B cellslncRNA RP11PI3K/Akt/mTOR pathwayneuromyelitis optica spectrum disease

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