Maternal-fetal immunity: presence of specific cellular hyporesponsiveness and humoral suppressor activity in normal pregnancy and their absence in preeclampsia.

P A Taufield, M Suthanthiran, K Ales, M Druzin, L M Resnick, J H Laragh, K H Stenzel, A L Rubin
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引用次数: 13

Abstract

The hypothesis that aberrant maternal-fetal immunity might lead to the development of preeclampsia was examined using mixed lymphocyte culture reactions (MLC) as an in vitro analogue of maternal-fetal immunity. Maternal lymphocytes and serum from five normal pregnant women differed significantly from lymphocytes and serum from five preeclamptics. Maternal cells from normal pregnancy responded appropriately to unrelated control cells, but demonstrated selective hyporesponsiveness to fetal cells in the MLC. Serum from normal pregnancy suppressed MLCs when maternal cells were responder cells (RC) and maternal cells or fetal cells were stimulator cells (SC), and did not inhibit MLCs where maternal cells were RC and control cells were SC. Maternal lymphocytes and serum from preeclamptics did not demonstrate cellular hyporesponsiveness or humoral suppressor activity. Our findings support the notion that specific cellular hyporesponsiveness and humoral suppressor activity is responsible for normal pregnancy; absence of such adaptive immunity might lead to the development of preeclampsia.
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母胎免疫:正常妊娠中存在特异性细胞低反应性和体液抑制活性,而子痫前期不存在。
利用混合淋巴细胞培养反应(MLC)作为母体-胎儿免疫的体外模拟物,对异常母胎免疫可能导致子痫前期发展的假设进行了检验。5例正常孕妇的外周血淋巴细胞和血清与5例子痫前期孕妇的外周血淋巴细胞和血清有显著差异。来自正常妊娠的母细胞对不相关的对照细胞有适当的反应,但在MLC中对胎儿细胞表现出选择性的低反应。当母细胞为反应细胞(RC),母细胞或胎儿细胞为刺激细胞(SC)时,正常妊娠血清抑制MLCs,而当母细胞为反应细胞(RC)和对照细胞为SC时,正常妊娠血清不抑制MLCs。子痫前期孕妇淋巴细胞和血清不表现出细胞低反应性或体液抑制活性。我们的研究结果支持了特异性细胞反应性低下和体液抑制活性导致正常妊娠的观点;缺乏这种适应性免疫可能导致先兆子痫的发展。
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Pre-eclampsia in a second pregnancy. A clinical follow-up study of 260 women with hypertension in pregnancy. Beta blocker therapy in 125 cases of hypertension during pregnancy. Disposition of the adrenergic blocker metoprolol in the late pregnant women, the amniotic fluid, the cord blood and the neonate. Maternal-fetal immunity: presence of specific cellular hyporesponsiveness and humoral suppressor activity in normal pregnancy and their absence in preeclampsia.
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