Th1 induced chronic inflammatory reactions in the fetal- maternal interface, placental damage and endothelial dysfunction by secreting the amounts of TNF-α, IFN-γ, IL- 1β, and IL- 12 (58).Preeclamptic symptoms such as elevated blood pressure, proteinuria and renal function abnormalities occur in pregnant mice after Th1 cell importation (59). This evidence concerns the gene TNF and endothelial dysfunction.