| publication name | The role of regulatory T cells in preeclampsia |
|---|---|
| Authors | Neveen A Abedel Hafeez · Mona El-Toukhy Fouda · Eman R Abdel Gawad · Tamer Assar · Amira I Mansour |
| year | 2014 |
| keywords | |
| journal | THE EGYPTIAN JOURNAL OF IMMUNOLOGY / EGYPTIAN ASSOCIATION OF IMMUNOLOGISTS |
| volume | 21 |
| issue | 1 |
| pages | 45-55 |
| publisher | Not Available |
| Local/International | International |
| Paper Link | Not Available |
| Full paper | download |
| Supplementary materials | Not Available |
Abstract
Preeclampsia is a multisystem disorder of unknown cause that is unique to human pregnancy affecting about 7-10% of pregnant women. CD4+CD25(bright) regulatory T (Treg) cells have been identified as a principle regulator of tolerance during pregnancy. The aim of this study was to demonstrate the change of peripheral CD4+CD25(bright) regulatory T lymphocytes in normal pregnancy and preeclampsia, and to explore its role in the pathogenesis of preeclampsia. We determined CD4+CD25(bright) Treg cells in the peripheral blood using flow cytometry and forkhead box P3 (FoxP3+) cells at the peripheral blood using real time PCR. 30 preeclamptic cases (group 1), 10 normal pregnancy subjects (group 2) and 10 non-pregnant healthy controls (group 3) were included. There was a highly significant decrease as regards Treg count and percentage in preeclamptic cases compared to normal pregnancy subjects (P < 0.001), decrease in preeclamptic cases compared to non-pregnant healthy controls (P < 0.001) and a significant increase in normal pregnancy subjects compared to non-pregnant healthy controls (P < 0.05). There was a statistically significant decrease as regards RQ of foxp3 gene expression in preeclamptic cases compared to normal pregnancy subjects (P < 0.001). There was no significant correlation between RQ and studied variables in preeclamptic cases (P > 0.05). These findings suggest that the number of Treg cells are decreased in preeclampsia, and this decrease may break the maternal tolerance to the fetus.