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Comparison of Immunosuppressive Properties of Hydatidiform Mole Decidua and Trophoblast Extracts
Author(s) -
Bennett William A.,
Brackin Martha N.,
Long Cecil A.,
Cowan Bryan D.
Publication year - 1996
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/j.1600-0897.1996.tb00144.x
Subject(s) - decidua , trophoblast , placenta , biology , andrology , fetus , medicine , endocrinology , microbiology and biotechnology , immunology , pregnancy , genetics
PROBLEM: The immunologic privilege afforded the fetus relies upon immunoregulation within the maternal‐fetal interface. Trophoblast and decidua‐derived immunoregulatory factors enforce this privilege by locally suppressing maternal responses to trophoblast antigens. The relative contribution of trophoblast or decidua immunosuppressive factors to pregnancy immunotolerance are not well characterized. The purpose of this study was to compare the suppressive effects of hydatidiform mole trophoblast and decidua extracts on interleukin‐2‐dependent proliferation. METHOD: Tissue extracts were prepared from hydatidiform mole trophoblast and decidua following uterine evacuation. Samples were submitted to interleukin‐2‐dependent and ‐independent cell proliferation assays. RESULTS: Hydatidiform mole trophoblast extract significantly ( P < 0.05) suppressed interleukin‐2‐dependent proliferation but did not affect interleukin‐2‐independent cell proliferation. In contrast, molar decidua extract suppressed both cell lines. CONCLUSIONS: Human hydatidiform mole trophoblast contains factor(s) that specifically abrogate interleukin‐2‐dependent clonal expansion of murine cytotoxic T‐cells. In contrast, extracts of molar decidua suppressed both interleukin‐2‐dependent and ‐independent responses. This indicates that the trophoblast antagonizes critical interleukin‐2‐mediated immunologic responses, but that the decidua uses nonspecific antiproliferative mechanisms for immunoregulation.