Preeclampsia and fetal growth restriction remain important causes of maternal and perinatal morbidity and mortality. In these conditions, a deficiency in regulatory T (Treg) cells, a specialized subset of lymphocytes, has been observed. Treg cells prevent maternal immune rejection of the fetus, but also contribute to vascular homeostasis in non-pregnant rats. We hypothesized that a reduced Treg cell population would cause inflammation and uterine artery dysfunction during pregnancy. Using the Foxp3-DTR Treg cell depletion mouse model, we investigated how Treg cell depletion in early pregnancy affected maternal vascular function in pregnancy, as well as fetal growth. Treg cell depletion affected uterine artery function on day 10.5 post coitum, as measured by wire myography and ultrasound biomicroscopy. Pro-inflammatory cytokines were increased, as well as the rate of fetal resorption. Furthermore, there was greater nitric oxide regulation of maternal mean arterial pressure. In late gestation, fetuses were growth restricted, and uterine and umbilical artery function is perturbed, as measured by ultrasound biomicroscopy. We demonstrate an essential role for Treg cells in maternal vascular function in pregnancy. Given the severe implications of preeclampsia on the future health of the mother and her baby, investigation of therapeutic strategies targeting Treg cells offers a promising intervention.