南方医科大学学报 ›› 2015, Vol. 35 ›› Issue (06): 848-.

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重度子痫前期PIBF的表达及其与免疫耐受失衡的关系

林 靓,黄云鹏,余艳红,杨 茵   

  • 出版日期:2015-06-20 发布日期:2015-06-20

Expression of progesterone-induced blocking factor in severe preeclampsia and its
association with immune tolerance imbalance

  • Online:2015-06-20 Published:2015-06-20

摘要: 目的探讨重度子痫前期胎盘及外周血孕酮诱导封闭因子(PIBF)表达情况及其与免疫耐受失衡的关系。方法选取2012
年1月~12月期间早发型重度子痫前期(EOPE)25例,晚发型重度子痫前期(LOPE)22例,对照组25例,收集产前外周血与产后
胎盘。用免疫组织化学(SABC法)检测胎盘PIBF的表达及定位,ELISA试剂盒检测血清PIBF水平,流式细胞仪检测外周血中
Th1和Th2细胞百分率,计算Th1/Th2比值。结果胎盘PIBF表达于蜕膜组织、合体滋养层细胞和部分绒毛滋养层细胞。血清
PIBF水平在EOPE组为213.58±44.93 ng/ml,LOPE组为243.00±61.19 ng/ml,对照组为273.91±48.57 ng/ml。三组间血清PIBF
含量、Th1/Th2比值和胎盘PIBF-IOD值差异均有统计学意义(P<0.05)。EOPE组和对照组相比,血清PIBF降低、胎盘PIBF表达
量(PIBF-IOD)减少、外周血Th1/Th2比值增高(P<0.05)。重度子痫前期孕妇血清PIBF与胎盘PIBF-IOD呈正相关关系,与外周
血Th1/Th2呈负相关关系(P<0.05)。但只有EOPE组血清PIBF与24h尿蛋白定量呈负相关关系(P<0.05)。结论PIBF介导的
免疫耐受失衡可能参与重度子痫前期发病机制。PIBF是妊娠诱发淋巴细胞分泌的免疫调节抑制因子及重度子痫前期的保护
因素,有望成为新的治疗靶点。

Abstract: Objective To explore progesterone-induced blocking factor (PIBF) expression in the placenta and blood of patients
with severe preeclampsia and its relationship with immune tolerance imbalance. Methods Forty-seven patients admitted
between January and December, 2012 were enrolled in this study, including 25 patients with early-onset severe preeclampsia
(EOPE) and 22 with late-onset severe preeclampsia (LOPE), with 25 women with normal pregnancy serving as control group.
The antenatal blood and postpartum placenta were collected for immunohistochemical staining to detect PIBF expression in
the placenta and for testing serum PIBF level using ELISA. Flow cytometry was used to detect the percentage of circulating
Th1 and Th2 cells and the Th1/Th2 ratio was calculated. Results PIBF was expressed in decidual cells, syncytiotrophoblasts
and partial cytotrophablasts. The serum PIBF levels were 213.58 ± 44.93 ng/ml in EOPE group, 243.00 ± 61.19 ng/ml in LOPE
group and 273.91±48.57 ng/ml in control group. There were significant differences in serum PIBF, blood Th1/Th2 and placenta
PIBF-IOD among the 3 groups (P<0.05). EOPE group had significantly lower serum PIBF, lower llacental PIBF quantity
(PIBF-IOD) and higher blood Th1/Th2 than the control group (P<0.05). Serum PIBF in women with severe preeclampsia was
positively correlated with placenta PIBF-IOD and negatively with blood Th1/Th2 ratio (P<0.05), but a negative correlation
between serum PIBF and 24-hour urinary protein was found only in EOPE group (P<0.05). Conclusion The immune tolerance
imbalance mediated by PIBF may participate in the pathogenesis of severe preeclampsia. PIBF, the immune suppressor
secreted by lymphocytes of pregnancy women, is also a protective factor against severe preeclampsia, which is expected to be
a new target in therapy.