Background: The imbalance of Treg/Th17 cells is an important pathogenic factor for immune thrombocytopenic purpura (ITP). We previously reported miR-125a-5p targeted CXCL13 and participated in the process of ITP. In the present study, the role of miR-125a-5p in regulating Treg/Th17 ratio and its potential molecular mechanism were investigated.
Method: A total of 30 adults with ITP and 30 healthy subjects were included. MEG3 expression in peripheral blood derived CD4+ T cells from ITP patients and healthy subjects were detected by real-time PCR. In vitro experiments, the effects of inhibiting or overexpressing MEG3 on the expression of miR-125a-5p, Foxp3 and ROTγt in CD4+ T cells were investigated.
Results: MEG3 expression was increased in CD4+ T cells of patients with ITP. Dexamethasone decreased MEG3 expression level of CD4+ T cells in vitro. MEG3 directly interacted with miR-125a-5p and MEG3 overexpression inhibited miR-125a-5p expression in CD4+ T cells exposed to dexamethasone. MEG3 down-regulation or miR-125a-5p overexpression promoted Foxp3 expression and inhibited RORγt expression.
Conclusion: MEG3 interacted with miR-125a-5p and inhibited its expression, and MEG3/miR-125a-5p contributed to induce immune imbalance of Treg/Th17 in ITP.
Keywords: Chemokine; Immune thrombocytopenia; Lymphocytes; miR-125-5p.
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