Our preliminary **data** suggest that infection with P. gingivalis induces loss of CD56 + dNK cells and an increase in CD16 + dNK cells in the first trimester. The ratio of CD16 + cells to CD56 + cells increases to 0.63 with infection versus 0.32 in control animals, and to a lesser extent so does the ratio of NKp46 + cells to CD56 + cells with infection (0.24) versus control (0.20), indicating a shift towards an activated phenotype [85,86]. There is evidence that CD56 bright cells have a crucial role in implantation, trophoblast migration, and spiral artery remodeling [64], and that these cells closely associate with dMΦ and decidual vessels in the first trimester [87,88].