Trophoblast growth / invasion of the uterine endometrium are critical events during placentation and are tightly regulated by factors produced within the trophoblast-endometrial micro-environment. Deficiencies in placentation can result in early miscarriage or pre-eclampsia and intrauterine growth restriction leading to impaired fetal health. The latter has been linked to major adult health disorders. Interleukin-11 (IL-11) is essential for blastocyst implantation in mice. In humans, IL-11 and its receptor IL-11 receptor alpha (IL-11R) are maximally expressed in the decidua and chorionic villi during early pregnancy; however the role of IL-11 in trophoblast function is unknown. Therefore, we examined whether IL-11R is expressed in human first trimester implantation sites and whether IL-11 influences proliferation and migration of a human EVT-hybridoma cell-line and primary EVT cells, used as models for EVT. Immunoreactive IL-11R localized to subpopulations of interstitial and endovascular EVT cells in vivo. In EVT cells in vitro, IL-11: i) stimulated phosphorylation of signal transducer and activator of transcription (STAT)-3 ii) was without effect on EVT cell proliferation (iii) stimulated significant migration of EVT-hybridoma cells (no endogenous IL-11) whereas in primary EVT, blocking endogenous IL-11 inhibited EVT migration by 30–40%. These data demonstrate that IL-11 stimulates human EVT migration but not proliferation likely via STAT-3, indicating an important role for IL-11 in placentation.