Mice ablated for the gene encoding the transcription factor Nfil3 lack peripheral natural killer (NK) cells but retain tissue-resident NK cells, particularly in mucosal sites, including virgin uterus. We undertook a time course histological study of implantation sites from syngeneically (Nfil3^−/−) and allogeneically (BALB/c) mated Nfil3^−/− females. We also examined implantation sites from Rag2^−/−Il2rg^−/− females preconditioned by adoptive transfer of Nfil3^−/− marrow or uterine cell suspensions to identify the Nfil3^−/− pregnancy aberrations that could be attributed to nonlymphoid cells. Uterine NKs (UNKs) reactive and nonreactive with the lectin Dolichos biflorus agglutinin (DBA) differentiate, localize, and mature within Nfil3^−/− implantation sites, although at reduced abundance. The DBA nonreactive UNK cells were enriched following Nfil3^−/− marrow transplantation. Uterine lumen closure, early embryonic development, and differentiation of antimesometrial decidua were delayed in Nfil3^−/− implantation sites. Major disturbances to the decidual-trophoblast interface that did not lead to fetal death were attributed to NFIL3 deficiency in trophoblast. At midgestation, vessels of the placental labyrinth were enlarged, suggestive of reduced branching morphogenesis. A major term complication in most Nfil3^−/− × Nfil3^−/− pregnancies but not Nfil3^−/− × Nfil3 ^/− pregnancies was dystocia. These studies highlight the differentiation potential and functions of Nfil3^−/− UNK cell progenitors and illustrate that much of the implantation site histopathology associated with this strain is due to Nfil3 deletion in nonlymphoid cell lineages.