Immunological protection of the fetus is based on a complex mechanism in which communication between the various steps is accomplished via cytokines. This study attempts to find the missing link between progesterone-dependent and cytokine-mediated immunomodulation. In the presence of progesterone, pregnancy lymphocytes produce a 34-kD protein, the progesterone-induced blocking factor (PIBF). PIBF blocks natural killer cell (NK) activity in vitro and displays an antiabortive effect in mice. In this study we have shown that PIBF is present on lymphocytes of healthy pregnant women, but not on those from pathological pregnancies and NK activity is inversely correlated to the rate of PIBF positivity of the lymphocytes. Additionally, our studies revealed that PIBF inhibits the transcription of interferon-γ (IFNγ) in activated human lymphocytes. On the other hand, PIBF induces a significant increase of Th2-type cytokine production by mitogen-activated murine spleen cells. PIBF affects antibody production by B cells. It induces concanavalin A (ConA)-binding IgG production by hybridoma cells. ConA reactivity reflects the presence of nonprecipitating asymmetric antibodies, which might contribute to the success of gestation by blocking effective immune responses. Our data suggest that PIBF reduces cell-mediated responses via altering the cytokine pattern during pregnancy.
|Original language||English (US)|
|Number of pages||5|
|State||Published - Jan 1 1995|
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