Investigation of T assistant-22 (TH22) and T assistant-17 (TH17) cells in preeclamptic placentas

Objective: Preeclampsia is one of the most common pregnancy complications during pregnancy. As the Extravillous Trophoblast (EVT) cells invade the maternal spiral arteries and remodel the vessels, it continues to provide all the metabolites necessary for embryo development from the mother. The balance of the maternal-fetal immune system during and after implantation is important for controlling EVT invasion. Helper T cells (Th) can cause the decidual microenvironment to become proinflammatory with the cytokines they secrete. In this study, the role and localization of Th17 and Th22 cells, which are involved in the proinflammatory response in the immune system, RORγ (RAR-related Orphan Receptor Gamma) and AHR (Aryl hydrocarbon receptor) proteins, and CD4 (Cluster of Differentiation 4) protein specific to helper T cells in preeclamptic and normal placental tissues was investigated. Method: Hematoxylin-Eosin staining was performed for the morphological analysis of preeclamptic placentas. The protein amounts of RORγ and AHR proteins in preeclamptic and control placentas were quantitatively determined by Western Blot (WB) method. By using immunofluorescence (IF) method, expression intensities and localization of Th17 and Th22 cells in preeclamptic and control placenta were determined by RORγ, AHR and CD4 staining. Results: As a result of WB experiments, a statistically significant increase was found in the amount of AHR protein in the preeclampsia group compared to the control group (p≤ 0.05). There was no statistical difference between the groups in the amount of RORγ protein (p ≥ 0.05). Cells with CD4 and AHR immunofluorescence staining in the term placenta were found to be more numerous in the decidua when compared to the control group in the preeclampsia group. No difference was detected in the expression of cells showing RORγ staining. Conclusion: Th22 cells with a statistically increased expression may play a role in the immune balance disorder in preeclampsia.