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首页> 外文期刊>Journal of Reproductive Immunology >The unique pathophysiology of early-onset severe preeclampsia: role of decidual T regulatory cells.
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The unique pathophysiology of early-onset severe preeclampsia: role of decidual T regulatory cells.

机译:早发型重度子痫前期的独特病理生理:蜕膜T调节细胞的作用。

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Immunological mechanisms play a pivotal role in the pathophysiology of preeclampsia. T regulatory cells (Treg cells, FoxP3(+)) suppress the cytotoxic T cell (CD8(+)) and natural killer (NK) cell response, thereby promoting immunological tolerance to the fetus. In peripheral blood, Treg cells are elevated during pregnancy, decrease throughout gestation, and are decreased in preeclampsia. To determine their role at the implantation site, we characterized the proportion of decidual Treg and CD8+ cells, and compared these with placental histology, villous sFlt expression, and chorionic trophoblast apoptotic index in normal and preeclamptic pregnancies. Decidua from first (n=5) and second (n=4) trimester terminations and chorioamniotic membranes, containing decidua, from term deliveries (n=14), early-onset (34 weeks) (n=14) severe preeclampsia were evaluated. Immunohistochemistry for CD3, CD8, and FoxP3 was performed: CD8(+) and FoxP3(+) cells were calculated as a proportion of CD3(+) cells. Placental tissue was evaluated for villous hypermaturity and sFlt staining. Chorioamniotic membranes were evaluated, via TUNEL assay, for chorionic trophoblast apoptosis. Decidual Treg cells were seen to peak in second trimester and decrease with advancing gestational age and were lower in early-onset (0.46%) compared with late-onset severe preeclampsia (3.34%) and term pregnancies (5.21%). The proportion of CD8(+) cells was higher in cases of severe preeclampsia. Early-onset severe preeclamptic cases had the highest sFlt score, placental insufficiency score, and apoptotic index. Our data suggest that early-onset severe preeclampsia has a unique pathophysiology involving defective immunoregulatory pathways, potentially causing vascular and trophoblast damage at the implantation site.
机译:免疫机制在先兆子痫的病理生理中起关键作用。 T调节细胞(Treg细胞,FoxP3(+))抑制细胞毒性T细胞(CD8(+))和自然杀伤(NK)细胞反应,从而促进对胎儿的免疫耐受。在外周血中,Treg细胞在怀孕期间升高,在整个妊娠过程中降低,在子痫前期中降低。为了确定它们在植入部位的作用,我们对蜕膜Treg和CD8 +细胞的比例进行了表征,并将其与胎盘组织学,绒毛sFlt表达和绒毛膜滋养细胞凋亡指数进行了比较。足月分娩(n = 14),早发( 34周)(n = 14)严重子痫前期。进行了CD3,CD8和FoxP3的免疫组织化学:计算CD8(+)和FoxP3(+)细胞占CD3(+)细胞的比例。评估胎盘组织的绒毛过成熟和sFlt染色。通过TUNEL测定法评价绒膜羊膜的绒毛膜滋养细胞凋亡。与晚期迟发严重子痫前期(3.34%)和足月妊娠(5.21%)相比,蜕膜Treg细胞在孕中期见高峰,并随着孕龄的增加而减少,早发时(0.46%)较低。严重先兆子痫患者中CD8(+)细胞的比例更高。早发型重度子痫前期患者的sFlt评分,胎盘功能不全评分和凋亡指数最高。我们的数据表明,早期发作的严重先兆子痫具有独特的病理生理学,涉及不良的免疫调节途径,可能在植入部位引起血管和滋养细胞的损害。

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