Early-onset preeclampsia is preceded by abnormal placentation and impaired spiral artery remodelling, and often results in fetal growth restriction. Foxp3+ regulatory T (Treg) cells, a specialised T cell subset with key roles in modulating inflammation, are deficient in many women with preeclampsia. Previously we showed, using acute transient depletion of Treg cells in early pregnancy elicited by diphtheria toxin (DT) administration to transgenic Foxp3-DTR mice, that Treg cells are critical for normal spiral artery remodelling and act to reduce the resistance index of the uterine artery in mid-gestation. Uterine natural killer (uNK) cells are also implicated in mediating decidual spiral artery remodelling, but whether Treg-uNK cells interactions are important for vascular remodelling is unknown. We therefore hypothesised that impaired spiral artery remodelling after Treg depletion is accompanied by altered uNK cell parameters. Mated Foxp3-DTR mice were injected with DT on gestational day 3.5 and 5.5 to deplete Treg cells and vehicle-treated Foxp3-DTR mice served as controls. On gestational day 10.5 uNK cell abundance was assessed by histochemical analysis and flow cytometry. Decidual sections stained with Dolichos Biflorus Agglutinin (DBA) lectin, which reacts with uNK cells, revealed a 20% decline in uNK abundance(P<0.001). Two distinct subsets of uNK cells have been described – tissue-resident and conventional (circulating) – each with distinct roles in angiogenesis and tissue remodelling. Flow cytometry was performed to further characterise the uNK decline using NK-cell associated markers, and the tissue residency marker CD49a to distinguish tissue-resident and conventional uNK subsets. Preliminary data revealed a decrease in conventional NK1.1+Nkp46+EOMES+CD49a- uNK cells within the uterus and decidua at mid-gestation following Treg depletion(P<0.05). These data suggest that Treg cells facilitate spiral artery remodelling through regulating conventional uNK cell abundance in the uterus and decidua. It will therefore be important to investigate decidual Treg cell-uNK cell interactions in women with preeclampsia.