Upregulation of miR-155 regulates group 2 innate lymphoid cells by targeting c-maf in allergic rhinitis.
Upregulation of miR-155 regulates group 2 innate lymphoid cells by targeting c-maf in allergic rhinitis.
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在过敏性鼻炎中，miR-155 的上调通过靶向 c-maf 来调节第 2 组先天淋巴细胞。
DOI：
10.1016/j.ejphar.2020.173564
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发表时间：
2020-09
影响因子：
5
通讯作者：
Meiqun Wang
中科院分区：
文献类型：
--
作者：
Yaqiong Zhu;Yuehui Liu;Xinhua Zhu;Zhi Wang;Meiqun Wang
Group 2 innate lymphoid cells (ILC2s) and Th2 type immune response are critically involved in the pathogenesis of allergic rhinitis (AR), and this pathological process is influenced by microRNAs-mediated post-transcriptional regulation. The present study investigated the adaptation and function of miR-155 in AR patients and mouse model. We found that significantly increased miR-155 expression (1.63 ± 0.12 vs. 0.92 ± 0.11 in human, and 1.68 ± 0.15 vs. 1.06 ± 0.06 in mice) and ILC2s activity in nasal mucosa and serum in AR patients and mice. Administration of miR-155 antagomir significantly reduced the activity of ILC2s in nasal mucosa, suppressed the production of Th2 cytokines in serum and nasal mucosa, and alleviated the airway inflammation and allergic symptoms in AR mice, while miR-155 agomir increased ILC2s activity and production of Th2 cytokines and induced airway inflammation and allergic symptoms in control mice. Meanwhile, the expression of transcriptional factor c-Maf (0.57 ± 0.05 vs. 0.37 ± 0.04) in nasal mucosa in AR mice, which was significantly recovered by miR-155 antagomir (0.56 ± 0.04). Treatment with miR-155 agomir decreased c-Maf expression in nasal mucosa in control mice. This synchronized with the similar pattern in the current observations that miR-155 regulated Th2 cytokine (IL-4, IL-5, IL-9 and IL-13) production, airway inflammation and allergic symptoms in AR mice. Together, upregulation miR-155 suppressed the expression of transcriptional factor c-Maf and was critically involved in the ILC2s activation, which contributed to the airway inflammation and allergic symptoms in AR.
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DOI：
10.4049/jimmunol.0900123
发表时间：
2009-05-15
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Xu J;Yang Y;Qiu G;Lal G;Wu Z;Levy DE;Ochando JC;Bromberg JS;Ding Y
通讯作者：
Ding Y
DOI：
10.4049/jimmunol.0803560
发表时间：
2009-04-15
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Lu TX;Munitz A;Rothenberg ME
通讯作者：
Rothenberg ME
miR-155 通过下调 CTLA-4 增加 Th 细胞的增殖反应，从而促进 Df1 诱导的哮喘
影响因子：
4.3
作者：
Zhang, Yingying;Sun, Entao;Lv, Kun
通讯作者：
Lv, Kun
DOI：
10.1126/science.1139253
发表时间：
2007-04-27
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Rodriguez A;Vigorito E;Clare S;Warren MV;Couttet P;Soond DR;van Dongen S;Grocock RJ;Das PP;Miska EA;Vetrie D;Okkenhaug K;Enright AJ;Dougan G;Turner M;Bradley A
通讯作者：
Bradley A
影响因子：
7.9
作者：
Inam, Asma;Shahzad, Muhammad;Javeed, Aqeel
通讯作者：
Javeed, Aqeel