RESUMEN
Abnormal immune response resulting from disordered T helper (Th)1/Th2 and Th17/regulatory T cells (Treg) cytokine expression has been demonstrated to serve an important role in the pathogenesis of preeclampsia (PE). However, the role of transcription factors regulating Th cell differentiation contributing to PE remain unclear. To determine whether a decrease in the expression of the T cell lineage transcription factor Tbet can restore immune balance and alleviate the systemic inflammatory response present in PE, 30 patients diagnosed with PE were assessed and compared with healthy pregnant controls. The expression of the transcription factors Tbet and retinoic acid receptorrelated orphan receptor (ROR)γt were increased in the peripheral blood mononuclear cells of PE patients compared with controls, consistent with the presence of abnormally high Tbet:GATA3 and RORγt:forkhead box (FOX) P3 ratios. The present study additionally identified a highefficiency, specific small interfering (si)RNA that can downregulate RORγt and Tbet mRNA levels and inhibit protein expression. This effective siRNA was transfected into activated CD4+ T cells derived from patients with PE to observe the changes to transcription factor expression and attempt to elucidate the regulatory mechanism of T cell subsets. It was identified that knockdown of RORγt induced increased expression of FOXP3 and that the ratios of RORγt:FOXP3 and interleukin (IL)17A:IL10 were subsequently decreased. The results suggested that siRNAmediated knockdown of Tbet regulated the immune balance of Th17/Tregs via changes to RORγt and FOXP3. When siRNA against RORγt and Tbet were used in combination, a stronger ability to regulate immune balance was observed. These results imply that Th1 and Th17type immunity is dominant in PE and that the siRNAmediated knockdown of certain Th1 and Th17 cell transcription factors may be an effective therapeutic target for promoting immune balance in CD4+ T cell subgroups and ameliorating local and generalized inflammation in PE.