Effect of fetal-maternal immune tolerance on pregnancy-induced hypertension
10.3969/j.issn.1000-484X.2017.09.025
- VernacularTitle:母-胎免疫调节机制在妊娠高血压综合征病理过程中的作用
- Author:
Lina LI
;
Zhenyu XU
;
Lina KONG
- Keywords:
Pregnancy-induced hypertension;
Fetal-maternal immune tolerance;
Placenta cytotrophoblast;
Cytokines;
Transcription factors
- From:
Chinese Journal of Immunology
2017;33(9):1398-1401
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To analyze the levels of immune cytokine in peripheral blood(PB) and the expressions of immune related transcription factors in placenta cytotrophoblast,which in patients with pregnancy-induced hypertension(PIH).And to explore the effect of fetal-maternal immune tolerance on pregnancy-induced hypertension.Methods:50 cases patients with PIH were selected as the observation group,and 40 healthy people were chosen as the control group.Enzyme-linked immunoassay(ELISA) was performed to detect the levels of IFN-γ,IL-4,IL-17 and TGF-β in peripheral blood.Quantitative Real-time PCR(RT-qPCR) and Western blot were used to analyze the mRNA expressions and protein levels of T-bet,GATA-3,RORC and Foxp3 in placenta cytotrophoblast,respectively.Results:①Compared with the control group,the IFN-γ and IL-17 levels in peripheral blood in the observation group were obviously higher and the TGF-β level was greatly lower(P<0.05).There was no significant difference of IL-4 level between the two groups(P>0.05),but the ratios of IFN-γ/ IL-4 and IL-17/TGF-β in the observation group were larger than that in the control group(P<0.05).②Compared with the control group,the mRNA expressios and protein levels of T-bet and RORC in the observation group were increased significantly(P<0.05),but that of GATA-3 and Foxp3 were decreased greatly(P<0.05).Thus,the ratios of T-bet/GATA-3 and RORC/Foxp3 in the observation group were significantly larger than that in the control group(P<0.05).Conclusion:PIH is occurred with the imbalance of Th1/Th2 and Th17/Treg,and it might be associated with the mechanism of fetal-maternal immune tolerance disorder that induced by Th cells.
