Preeclampsia is an important cause of maternal and perinatal morbidity and mortality, and increases the susceptibility of the mother and offspring to cardiovascular disease later in life. In preeclampsia, a deficiency in regulatory T (Treg) cells has been observed. Treg cells prevent maternal immune rejection of the fetus, and suppress inflammatory activation. We have shown they also contribute to uterine vascular function in pregnant mice (Care et al Hypertension 2018), consistent with emerging roles in systemic vascular homeostasis. However, the role of Treg cells in spiral artery remodelling in early placental development remains unclear. Uterine natural killer (uNK) cells are a specialised subset of innate immune cells, with a pivotal role in spiral artery remodelling during pregnancy. Although there is evidence of Tregs and NK cells communicating in the peripheral organs, whether and how they interact within the uterus during pregnancy is unknown. We hypothesise that Treg cell deficiency in early pregnancy will alter uterine natural killer cell (uNK) abundance, leading to impaired spiral artery remodelling and fetal growth restriction. Using transgenic Foxp3-DTR mice we can elicit selective depletion of FOXP3+ (Treg) cells to investigate the role of Treg cells in maternal vascular adaptations to pregnancy. In mid-pregnancy Treg cell depletion led to perturbed uterine artery function. Decidual spiral artery remodelling was impaired, evidenced by a smaller artery lumen area and smooth muscle actin retention, leading to a reduction in fetal weight in late gestation. Moreover, the abundance of uNK cells in the decidua was decreased in Treg-depleted mice compared to controls. However, administration of exogenous wild-type Treg cells restored uterine artery function, spiral artery remodelling and uNK cell abundance, demonstrating a causal role for Treg cell deficiency. We demonstrate an essential role for Treg cells in fetal growth and uteroplacental vascular function. Given the severe implications of preeclampsia on the future health of the mother and her offspring, investigation of therapeutic strategies targeting Treg cells may offer a promising target for intervention.