Prednisone may induce immunologic tolerance by activating the functions of decidual immune cells in early pregnancy
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Xiao-Qian Fu1, Jun-Ying Cai2, Qian-Yi Huang1, Dong-Ju Li3, Ning Li3 and Mu-Jun Li1
1Department of Reproductive Center, First Affiliated Hospital of Guangxi Medical University, Guangxi, China
2Department of Reproductive Center, Maternal and Child Health Hospital and Obstetrics and Gynecology Hospital of Guangxi Zhuang Autonomous Region, Guangxi, China
3Guangxi Medical University, Guangxi, China
Mu-Jun Li, email: email@example.com
Keywords: interleukin-17; prednisone; interleukin-10; Treg cells; Th17 cells
Received: May 18, 2017 Accepted: October 04, 2017 Published: October 31, 2017
The objective of this study was to investigate alterations in human first-trimester decidual immune cells (DICs) and relevant cytokines after treatment with prednisone. Decidual lymphocytes were treated with prednisone alone, cytokines alone or the combination of prednisone and cytokines. Levels of STAT3, STAT5, RORC and FOXP3 mRNA were assayed using quantitative real-time PCR, proportions of CD4+ T helper 17 (Th17) and CD4+ T regulatory (Treg) cells were measured using flow cytometry, and concentrations of interleukin (IL)-17A and IL-10 were determined using enzyme-linked immunosorbent assay. After treatment with prednisone alone, levels of STAT5 and FOXP3 mRNA were significantly higher than in untreated control cells (both P < 0.01), while levels of RORC mRNA were significantly lower than in controls (P < 0.05). Levels of STAT3 mRNA did not vary significantly with treatment. After treatment with prednisone alone, proportions of Th17/CD4+ cells and levels of IL-17A were significantly lower than in control cells, and proportions of Treg/CD4+ cells and levels of IL-10 significantly higher than in controls (all P < 0.01). Our results suggest that prednisone may improve pregnancy outcomes by restoring immunological homeostasis through up-regulation of STAT5 and FOXP3, induction of DIC differentiation into Treg cells, inhibition of DIC differentiation into Th17 cells, reduction of IL-17A secretion and induction of IL-10 secretion.
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