الفهرس 
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Abstract
Preeclampsia (PE) defined as a severe pregnancy complication characterized with a worldwide prevalence of 2–8% which plays a significant role in maternal and prenatal morbidity and mortality.
The aetio-pathogenesis of PE is not yet fully understood. It has been suggested that deficient implantation may lead to infertility, whereas inappropriate placentation to fetal growth restriction. However, pre-eclampsia results from placental dysfunction that alters maternal system progressing through a preclinical to a clinical stage ultimately leading to maternal manifestations of the disease.
There development of preeclampsia has a multifactorial there nature and is influenced by different factors such as fetal/paternal genetic and environmental risk factors. Although, there was intensive research efforts, preeclampsia etiology and pathogenesis of are not understood till now.
Abundant evidence suggests that the involvement of immunological factors is crucial in the causation of PE. Apparently an aberrant and persistent maternal systemic inflammatory response to pregnancy with cytokine-mediated endothelial damage plays an essential role in the pathogenesis of preeclampsia.
FoxP3, one of the X chromosome-encoded fork head transcription factor family, is a master control gene, requisite for the development and functioning of Tregs. FoxP3 is essential for the conversion of naïve T-cells to Tregs which are implicated in maintenance of successful pregnancy.
Till now there was limited studies evaluate the role of Foxp3 in human being. It has been demonstrated in mouse models that inactivation of Foxp3 results in a deficiency of Tregs, and notable organ specific Foxp3 is a major regulator for the development and function of Tregs. As deficiency of Foxp3 may impair the suppressive function of Tregs.
Several previous trails have found a relationship between Foxp3 gene expression and polymorphisms and autoimmune diseases, as autoimmune thyroiditis, allergic rhinitis, diabetes type I and systemic lupus erythematosus.
Zhou Jianjun et al., reported that Th1 type immunity was the predominant in pre-eclampsia with decreased expression of Foxp3 mRNA.
The decreased expression of Foxp3 in preeclampsia demonstrates that, the reduction of Tregs numbers may be associated with imbalance of immunologic tolerance between the mother and foetus, thereby participating in the pathogenesis of preeclampsia. Few published literatures on the FoxP3 variation from various geographic regions produced somewhat controversial conclusion.
This case control study was conducted at Antenatal care word and delivery room - Department of obstetrics and gynecology - Faculty of Medicine – Ain Shams University from 1st June 2021 until 15th August 2022. A total of 26 pre-eclamtic women and 26 ethnically matched healthy pregnant women as a control group aged between 18 and 40 years old of different gravidity and parity referred to labor ward for delivery either by vaginal delivery or cesarean section were enrolled to investigate the immunohistochemical expression of FoxP3 in placental tissue of PE patients.
Our study reported that, lower expression of FOXP3 IHC was statistically significant in group of preeclampsia compared with healthy control group.
We also found that gestational age at delivery was statistically significant lower and percentage of cesarean section was statistically significant higher in group of preeclampsia compared with healthy control group. On the other hand, there were no significant differences between study groups regarding maternal age, parity, history of previous abortions, cesarean sections and preeclampsia.
In conclusion, in women with high risk for development of preeclampsia, FOXP3 immunohistochemical expression could be evaluated and used as a predisposing factor of PE development. Due to its clinical importance, more randomized comparative clinical trials with larger sample size and more data are needed for further evaluation of other FOXP3 polymorphisms and mutations.