Significant pregnancy loss occurs in cattle during the early stages of embryogenesis and placentation. Several critical events occur in the first 3 to 4 weeks of gestation, and aberrations in any one of these events will prompt pregnancy loss. One such event is maternal recognition of pregnancy, when interferon-tau (IFNT) must be produced in sufficient quantities from the conceptus to prevent luteolysis and modify uterine function to favor pregnancy. Epidermal growth factor (EGF) is produced by the uterus and is a recognized embryotrophic factor. Specific activities in bovine embryos include improving rates of bovine embryo development and increasing trophectoderm (TE) proliferation. This study examined whether EGF affects IFNT expression. A stable bovine TE cell line (CT1) was maintained in Dulbecco’s Modified Eagle’s Medium (DMEM). Cells were serum-starved and then exposed to various concentrations of human recombinant EGF. Total cellular RNA was extracted, and quantitative reverse transcription PCR was completed using IFNT-specific primers and ribosomal protein S9 (RPS9; internal control). Data were analyzed by ANOVA. In the first study, a 6 h dose response was completed (n = 3 replicate studies). Supplementation with 100 ng/mL EGF increased (P < 0.05) IFNT transcript abundance when compared with controls (2.3 ± 0.8 fold effect). Exposure to 1 or 10 ng/mL EGF did not affect IFNT transcript abundance. In the second study, a 24 h dose-response was completed (n = 3 replicate studies). A trend in increased IFNT mRNA abundance was evident (P = 0.07) when CT1 cells were supplemented with 1 ng/mL EGF (2.0 ± 1.5 fold vs. controls). Incubation with either 10 or 100 ng/mL EGF increased (P < 0.05) IFNT transcript abundance when compared with controls (2.6 ± 0.8 and 3.6 ± 1.4 fold effect, respectively). Moreover, the 100 ng/mL effect was more pronounced than the 1 ng/mL effect (P = 0.06; 1.75 ± 0.7 fold). These outcomes implicate EGF as a mediator of IFNT expression, and provide further evidence of how the maternal system may control IFNT production and other developmental events during early pregnancy in ways that dictate pregnancy retention or failure.