Toxoplasmosis can cause abortion in pregnant humans and other animals; however, the mechanism of abortion remains unknown. C-C chemokine receptor type 5 (CCR5) is essential for host defense in T. gondii infection. To investigate the relationship between CCR5 and abortion in toxoplasmosis, we inoculated wild-type and CCR5-deficient (CCR5-/-) mice with T. gondii tachyzoites intraperitoneally on day 3 of pregnancy (E3). The pregnancy rate decreased as pregnancy progressed in the infected wild-type mice. Histopathologically, no inflammatory lesions were observed in the fetoplacental tissues. Although the wild-type mice showed a higher parasite burden at the implantation sites than the CCR5-/- mice at E6 (3 days post-infection, dpi), T. gondii antigen was detected only in the uterine tissue, not in the fetoplacental tissues. At E8 (5 dpi), the embryos in the infected wild-type mice showed poor development compared with the infected CCR5-/- mice and apoptosis was observed in poorly developed embryos. Compared with the uninfected mice, the infected wild-type mice showed increased CCR5 expression at the implantation site at E6 and E8. Furthermore, analyses of mRNA expression in the uterus of non-pregnant and pregnant mice suggested that lack of the CCR5 gene and downregulation of TNF-α and CCL3 expression at E6 (3 dpi) are important factors for maintenance of pregnancy following T. gondii infection. These results suggested that CCR5 signaling is involved in embryo loss in T. gondii infection during early pregnancy, and that apoptosis is associated with embryo loss rather than direct damage to the fetoplacental tissues.