Preeclampsia is a pregnancy complication associated with impaired spiral artery remodeling. Serum concentrations of C1q are decreased in some women with preeclampsia. C1q is produced by trophoblast cells and macrophages that, along with uterine natural killer (uNK) cells, facilitate spiral artery remodeling. Regulatory T (Treg) cells are anti-inflammatory cells which maintain immune homeostasis during these processes. The significance of maternal C1q deficiency on pregnancy outcomes has not been investigated. We hypothesized that maternal C1q deficiency would impair spiral artery remodeling and fetal growth which may be associated with a reduced Treg cell abundance. Female mice with a null mutation in C1qa (C1qa-/-) were mated to BALB/c male mice. Treg cell proportions were assessed using flow cytometry. Blood pressure was measured before and during pregnancy using tail cuff plethysmography. Ultrasound bio-microscopy assessed uterine artery function. Wild-type C57BL/6 female mice mated to BALB/c males were controls, and significant differences (P<0.05) were assessed. C1qa-/- dams had a 25% reduction in Treg cell abundance in mesenteric lymph nodes on day 3.5 post coitum. At mid-gestation, decidual artery lumen area was reduced by 41%, indicative of impaired spiral artery remodeling, and uNK cell abundance was reduced by 11%. C1qa-/- dams demonstrated uterine artery dysfunction with a ≥16% increase in artery resistance and pulsatility indices at mid-gestation. Mean arterial pressure (MAP) was not different between C1qa-/- and wild-type dams before or at mid-gestation. However, in late-gestation, MAP decreased in wild-type mice, but not in C1qa-/- mice, indicative of failed haemodynamic adaptations to pregnancy. In late-gestation, fetal weight and fetal: placental weight ratios were reduced in C1qa-/- dams by ≥10% compared to controls. In conclusion, maternal C1q deficiency has adverse consequences for maternal vascular adaptations to pregnancy and the underlying mechanism likely involves Treg cells. These data suggest a key role for C1q in uterine vascular remodeling.