妊娠肝内胆汁淤积症患者的胎儿淋巴细胞研究

目的探讨胎儿淋巴细胞在妊娠肝内胆汁淤积症(ICP)发病中的作用。方法采用单向混合淋巴细胞反应法,检测20例ICP患者(ICP组)及20例正常孕妇(对照组)的脐血胎儿淋巴细胞与母体外周血已灭活的淋巴细胞、皮肤组织可溶性抗原、蜕膜组织可溶性抗原的增殖反应情况。结果(1)ICP组脐血胎儿淋巴细胞与母体已灭活的淋巴细胞混合反应中,胎儿淋巴细胞的增殖反应程度为2．75±0．36,显著高于对照组的1．45±0．19,两组比较,差异有统计学意义(P＜0．05);(2) ICP组脐血胎儿淋巴细胞与母体蜕膜组织可溶性抗原混合反应中,胎儿淋巴细胞的增殖反应程度为1．45±0．19,显著高于对照组的0．67±0．24,两组比较,差异有统计学意义(P＜0．05);(3)ICP组脐血胎儿淋巴细胞与母体皮肤组织可溶性抗原反应中,胎儿淋巴细胞的增殖反应程度为1．22±0．44,显著高于对照组的0．66±0．27,两组比较,差异有统计学意义(P＜0．05)。结论胎儿淋巴细胞可能是ICP发病过程中的主要效应细胞之一;母-胎间免疫失衡是ICP发病的重要机制之一。

Study of fetal lymphocyte of intrahepatic cholestasis of pregnancy

OBJECTIVE: To explore effect of fetal lymphocyte on pathogenesis of intrahepatic cholestasis of pregnancy (ICP). METHODS: Twenty pregnant women with ICP and 20 normal pregnant women were enrolled in the study. The single mixed lymphocyte culture/reaction (MLC/MLR) was conducted using inactive lymphocyte obtained from maternal peripheral blood and lymphocyte of cord blood from fetus. Antigen-induced-lymphocyte-proliferation-reaction was used for dermic soluble antigen and decidual soluble antigen obtained from maternal blood and cord blood from fetus. The intense of proliferation was calculated and compared between normal and ICP-complicated pregnancies. RESULTS: (1) The level of intense of proliferation of fetal lymphocyte was significantly increased in ICP group 2.75 +/- 0.36 than those of normal control group 1.45 +/- 0.19 in single mixed lymphocyte culture (P < 0.05). (2) The level of intense of proliferation of fetal lymphocyte was significantly increased in ICP group 1.45 +/- 0.19 than those of normal control group 0.67 +/- 0.24 in decidual soluble antigen induced lymphocyte proliferation reaction (P < 0.05). (3) The level of intense of proliferation of fetal lymphocyte was significantly increased in ICP group (1.22 +/- 0.44) than those of normal control group (0.66 +/- 0.27) in dermic soluble antigen induced lymphocyte proliferation reaction. CONCLUSIONS: (1) The fetal lymphocyte may be one of the effector cells in pathogenesis of ICP. (2) The disturbance of fatal-maternal immune-tolerance is one of the important mechanisms underlying ICP.