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MicroRNA-142-3p inhibits IFN-γ production via targeting of RICTOR in Aspergillus fumigatus activated CD4+ T cells

  
@article{ATM31948,
	author = {Ning Ma and Ting Wei and Bin Wang and Xiaohua Jiang and Lin Zhou and Renqian Zhong},
	title = {MicroRNA-142-3p inhibits IFN-γ production via targeting of RICTOR in  Aspergillus fumigatus activated  CD4 +  T cells},
	journal = {Annals of Translational Medicine},
	volume = {7},
	number = {22},
	year = {2019},
	keywords = {},
	abstract = {Background: Aspergillus fumigatus (AFE) is a well-adapted, opportunistic fungus that causes a severe and commonly fatal disease, wherein IFN-γ is one of the most important protective cytokines. The aim of this study was to investigate the microRNA expression profile and explore the underlying mechanism during infection with AFE. 
Methods: CD4+  T cells were activated by co-culturing with dendritic cells (DCs), which were pre-treated with AFE. Next, we performed microRNA microarray expression profiles of activated and control T cells, following which, miRNA-142-3P was selected. To explore the effect of miR-142-3P on T cell activation, miRNA-142-3P expression was disrupted by transient transfection with miR-142-3P mimic or inhibitor. Then, levels of RICTOR, phosphorylated AKT and IFN-γ were detected via Western blotting and qPCR respectively. We further used siRNA to decrease RICTOR expression and determined the role played by RICTOR in miR-142-3P mediated-IFN-γ expression by qPCR following AFE-mediated T cell activation. 
Results: The heat-map of miRNA expression profiles showed that 54 microRNAs (miRNAs) were filtered, the levels of which, were significantly different between CD4+  T cells activated by AFE and control T cells, in which microRNA-142-3 was involved. Forced expression of miRNA-142-3P dramatically suppressed RICTOR levels, phosphorylated AKT and IFN-γ in AFE activated T cells. Conversely, loss of miRNA-142-3P elevated RICTOR levels, phosphorylated AKT and IFN-γ. Notably, RICTOR deficiency decreased AKT phosphorylation levels and IFN-γ secretion. 
Conclusions: Observations indicated that down-regulation of microRNA-142-3p enhanced IFN-γ expression, and did so by promoting RICTOR expression in CD4+  T cells activated by AFE.},
	issn = {2305-5847},	url = {http://atm.amegroups.com/article/view/31948}
}