The antiabortive effect of progesterone-induced blocking factor in mice is manifested by modulating NK activity.
Immunologic effects of progesterone are mediated by a protein named the progesterone-induced blocking factor (PIBF), which inhibits NK activity and displays an antiabortive effect in mice. Our previous data provide indirect evidence for the importance of PIBF in the maintenance of normal gestation. This study was aimed at investigating whether neutralization of endogenous PIBF production influences pregnancy outcome and if so, what are the mechanisms that participate in this process. Syngeneically pregnant Balb/c mice on Day 8.5 of pregnancy were injected ip with 0.3 mg/kg of RU 486 or with 0.5 mg of rabbit anti-PIBF IgG alone, or together with anti-NK monoclonal antibodies. Mice treated with the same amount of normal rabbit serum or untreated mice of similar gestational age were used as controls. On Day 10.5 the ratio of living and resorbed embryos and NK activity of the spleen cells were determined. In mice treated with anti-PIBF the ratio of resorbed fetuses was significantly higher than that in untreated controls. In RU 486-treated mice we also observed significantly increased resorption rate, which was associated with the inability of spleen cells to produce PIBF. Both anti-PIBF treatment and that with progesterone receptor blocker resulted in increased splenic NK activity. There was a positive relationship between NK activity and the rate of resorptions. All the above effects were corrected by simultaneous treatment with anti-NK or anti-NC (natural cytotoxic) antibodies. These data allow the conclusion that PIBF contributes to normal gestation in mice and that the effect of PIBF is manifested via blocking NK and/or NC activity.
Szekeres-Bartho
J
J
Department of Microbiology, University Medical School of Pecs, Hungary.
Par
G
G
Dombay
G y
Gy
Smart
Y C
YC
Volgyi
Z
Z
D000022:Abortion, Spontaneous / Q000276:immunology / Q000517:prevention & control*; D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology / Q000633:toxicity; D003602:Cytotoxicity, Immunologic / Q000187:drug effects; D005260:Female; D005327:Fetal Resorption / Q000139:chemically induced / Q000517:prevention & control*; D007694:Killer Cells, Natural / Q000276:immunology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D015735:Mifepristone / Q000494:pharmacology / Q000633:toxicity; D011247:Pregnancy; D011257:Pregnancy Proteins / Q000037:antagonists & inhibitors / Q000276:immunology / Q000502:physiology*; D011374:Progesterone / Q000502:physiology*; D011817:Rabbits; D013491:Suppressor Factors, Immunologic / Q000037:antagonists & inhibitors / Q000276:immunology / Q000502:physiology*
D000911:Antibodies, Monoclonal; C491677:Pibf1 protein, mouse; D011257:Pregnancy Proteins; D013491:Suppressor Factors, Immunologic; D015735:Mifepristone; D011374:Progesterone