Repository of Research and Investigative Information

Repository of Research and Investigative Information

Hormozgan University of Medical Sciences

Research project #1197

(2014) بررسی نقش واریانتهای ژن FOXP3 ((rs2232365, rs3761548, rs3761547, rs4824747 در استعداد ابتلا به بیماری پراکلمسی. completed.

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Evaluation of 4 single nucleotide polymorphisms (rs2232365, rs3761548, rs3761547, rs4824747) of FOXP3 gene as a risk factor in the genetic susceptibility to preeclampsia


Preeclampsia is a severe pregnancy complication characterized by hypertension and proteinuria after 20 weeks of gestation. Globally, preeclampsia affects 5–8% of pregnancies and contributes significantly to maternal and fetal morbidity and mortality (1). Despite intensive research efforts, the etiology and pathogenesis of preeclampsia and HELLP syndrome are not completely understood. The development of preeclampsia and HELLP syndrome is influenced by both maternal and fetal (paternal) genetic and environmental risk factors,suggesting their multifactorial inheritance (2) .Latest observations have led to the hypothesis that preeclampsia may in part be immune mediated.Normal pregnancy requires a relative maternal immune tolerance of the fetus. Adaptation of the maternal immune response to accommodate the semi-allogeneic fetus is necessary for pregnancy success, and disturbances in maternal tolerance are implicated in miscarriage.We know that women are at increased risk of preeclampsia in their first pregnancy,and with new partners (3). Emerging evidence suggests that an excessive maternal systemic inflammatory response to pregnancy with cytokine-mediated endothelial damage plays a crucial role in the pathogenesis of both disorders. The immune system in PE is changed with a shift towards Th1-type immunity ,where T lymphocytes producing proinflammatory cytokines that activate cytotoxic cells (Th1 lymphocytes) increase in concentration. The cells that are almost certainly the key regulators of this response are a distinct population of T cells known as regulatory T cells called Tregs (4)(5). Regulatory T cells (CD4+ CD25+ FOXP3+ Treg) are pivotal to the maintenance of self-tolerance and the control of immune homeostasis. Treg cells are characterized by their ability to suppress effector T cells of either TH1 or TH2 phenotypes involved in mediating inflammation.The mechanisms utilized by natural Tregs that have probably been examined and discussed the most are inhibitory cytokines (TGFβ, IL-10, IL-35), inhibitory receptors (CTLA4, LAG-3), cytotoxicity (Granzyme/Perforin) and metabolic disruption (6-11).Many studies show that CD4+ CD25+ FOXP3+ Treg cells are essential for suppressing immune responses and maternal tolerance of the conceptus :First, Treg cells accumulate in the decidua and are elevated in maternal blood from early in the first trimester

Item Type: Research project
Subjects: surgery gynecology and obstetrics
molecular Genetics
Divisions: Research Vice-Chancellor Department > Molecular Medicine Research Center
Depositing User: مرکز تحقیقات پزشکی مولکولی

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