O73. The role of Th17/Treg imbalance in normal pregnancy and pre-eclampsia

Abstract

Introduction The etiology and pathogenesis of pre-eclampsia are not yet fully understood. Many of the findings support a hypothesis that an inappropriate activation of immune system is associated with the development of this syndrome. Objectives The aim of the study was to estimate the prevalence of CD3 + CD4 + T lymphocytes producing IL-17, IL-2, IFN-and IL-4, as well as CD4 + CD25 + FoxP3 + Tregulatory cells (Tregs) in peripheral blood of patients with preeclampsia and healthy women in the third trimester of normal pregnancy. Furthermore, the purpose of our study was to assess the immunosuppressive activity of Treg cells of patients with preeclampsia in comparison with the controls. Methods Thirty four patients with preeclampsia and 27 healthy women in third trimester of pregnancy were included to the study. The percentage of CD4 + CD25 + FoxP3 + Treg cells and CD3 + CD4 + T lymphocytes with intracellular expressions of cytokines was estimated using monoclonal antibodies and flow cytometry. The in vitro functional assays were performed with the use of Treg Cells Isolation Kit and 3 H-thimidine. Results The percentages of T CD3 + CD4 + lymphocytes producing IL-17A were significantly higher in preeclampsia when compared to healthy normotensive pregnant women in the third trimester of normal pregnancy ( p + CD25 + FoxP3 + Treg cells was significantly lower in the study when compared to the control group ( p + CD4 + CD25 − T lymphocytes of patients with preeclampsia during in vitro assay without Treg cells and after the addition of autologous Tregs. In normal pregnancy the stimulation index of CD3 + CD4 + CD25 − T lymphocytes was significantly higher without Treg cells when compared to this response after addition of autologous Tregs ( p Conclusions The results obtained suggest the up-regulation of Th17 immune response in preeclampsia. It seems that the decreased number and function of Treg cells may be responsible for the activation of inflammatory response in this disorder. In preeclampsia the predominance of Th17 immunity can act through the modulation of Th1/Th2 immune response.