At the beginning of pregnancy, the ovarian steroid hormones 17β-estradiol (E2) and progesterone (P4) stimulate synthesis of growth factors from the uterine epithelium, including CSF-1 and leukemia inhibitor factor (LIF). LIF, acting on the luminal epithelium, is essential for blastocyst implantation and subsequent decidualization. CSF-1 recruits and regulates uterine macrophages, while also influencing the biology of uDCs. In addition, CSF-1 acts on decidual cells and trophoblastic cells (not shown). Macrophages play a largely immune role at this stage, while, as Plaks et al. (7) show in their current study in this issue of the JCI, uDCs are required for efficient decidualization. This decidualization process involves transformation of stromal cells into epithelioid-type cells at the site of blastocyst implantation on the antimesometrial side of the uterus. The decidual cells grow in an arc, via rapid proliferation and transformation, to surround the implanting embryo. After implantation is complete, the blastocyst is entirely surrounded by a primary decidual zone of polyploid cells and a secondary diploid decidual zone. Vascularization commences on the mesometrial side of the uterus via the growth of vascular sprouts from the uterine artery into the decidua, which results in vessels with large, dilated lumens through which maternal blood bathes the decidual nodule. As Plaks et al. report, uDCs located in the outer layers of the decidua regulate this vascularization in part through their synthesis of TGF-β1 and sFLT1. Ablation of uDCs results in a failure of decidual growth and resorption of the embryo, showing that uDCs are essential for a successful pregnancy.