Earlier data suggest that progesterone-induced blocking factor (PIBF) is involved
in implantation. The present study therefore aims to investigate the consequences
of functional PIBF deficiency during the peri-implantation period. CD1 female mice
were injected intraperitoneally with 2 μg anti-PIBF monoclonal antibody on days 1.5
and 4.5 of pregnancy. The number of implantation sites and resorption rates were recorded
on day 10.5. PIBF+ decidual NK cells and B cells were detected by immunohistochemistry
or immunofluorescence. Decidual and peripheral NK activity was assessed by flow cytometry.
A prime PCR array was used for determining the differential expression of genes involved
in lymphocyte activation and Th1 or Th2 differentiation in CD4+ and CD8+ spleen cells
from pregnant anti-PIBF-treated and control mice. Anti-PIBF treatment in the peri-implantation
period resulted in impaired implantation and increased resorption rates in later pregnancy.
The number of PIBF+ decidual NK cells decreased, while both decidual and peripheral
NK activity increased in the anti-PIBF-treated mice. B cells were absent from the
resorbed deciduas of anti-PIBF-treated mice. The genes implicated in T cell activation
were significantly downregulated in CD4+ and increased in CD8+ of the anti-PIBF-treated
animals. The gene for IL-4 was significantly downregulated in CD4+ cells while that
of IL-12A was upregulated in CD8+ cells of anti-PIBF-treated animals. These data suggest
that the lack of PIBF results in an impaired T cell activation, together with Th1
differentiation and increased NK activity, resulting in implantation failure.
