The fetal–placental unit is a semi-allograft and immunological recognition of pregnancy, together with the subsequent response of the maternal immune system, is necessary for a successful pregnancy. Dendritic cells (DC) show a biological plasticity that confers them special characteristics regulating both immunity and tolerance. Therapy employing DC proved to diminish the abortion in the DBA/2J-mated CBA/J females; however, the underlying mechanisms remain unknown. Here, we evaluated whether DC therapy influences the presence of immunoregulatory populations of cells at the fetal–maternal interface. To address this hypothesis, we analysed the pregnancy-protective CD8, γδ cell populations as well as transforming growth factor (TGF)-β1 and progesterone-induced blocking factor (PIBF) expression at the fetal–maternal interface from abortion-prone female mice that had previously received adoptive transfer of syngeneic DC. Syngeneic DC therapy induced an increase in the number of CD8 and γδ cells. Additionally, an upregulation of TGF-β1 and PIBF expression could be detected after DC transfer. We suggest that DC therapy differentially upregulates a regulatory/protective population of cells at the fetal–maternal interface. It is reasonable to assure that this mechanism would be responsible for the lower abortion rate.