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.
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Vol. 94 • No. 5