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- Title
MEG3 modulates TIGIT expression and CD4 + T cell activation through absorbing miR-23a.
- Authors
Wang, Jianhong; Liu, Xiangxiang; Hao, Caixia; Lu, Yingjuan; Duan, Xiaohui; Liang, Rong; Gao, Guangxun; Zhang, Tao
- Abstract
T cells are involved in bone marrow failure in aplastic anemia (AA). MEG3 is a long, non-coding RNA that can modulate target gene expression and T cell differentiation by acting as a microRNA sponge. Our previous study showed that T cell immunoglobulin and immunoreceptor tyrosine-based inhibition motif (ITIM) domain (TIGIT) plays a critical role in regulating CD4 + T cell functions. In this study, we found that MEG3 expression was significantly downregulated in CD4 + T cells derived from AA patients. MEG3 modulated CD4 + T cell proliferation and IFN-γ and TNF-α levels, as well as TIGIT, T-bet, and orphan nuclear receptor (RORγt) expression. Furthermore, MEG3 overexpression sequestered miR-23a and prompted TIGIT expression in CD4 + T cells. CD4 + T cells with MEG3 overexpression impeded expansion of Th1 and Th17 cells, restored the decreased red blood cell count, attenuated the increase in serum INF-γ and TNF-α levels, and lengthened median survival time, as well as upregulated mRNA levels of CD34, stem cell factor (SCF), and granulocyte/macrophage-colony-stimulating factor (GM-CSF) in bone marrow mononuclear cells of a mouse model. In conclusion, our study provides evidence that MEG3 regulated TIGIT expression and CD4 + T cell activation by absorbing miR-23a. These findings provide novel insight into autoimmune-mediated AA.
- Subjects
GRANULOCYTES; T cells
- Publication
Molecular & Cellular Biochemistry, 2019, Vol 454, Issue 1/2, p67
- ISSN
0300-8177
- Publication type
Article
- DOI
10.1007/s11010-018-3453-2