干预CD86协同刺激信号对母胎界面Th1/Th2型细胞因子转录调控及妊娠结局的影响  

Influence of Blockade of CD86 Costimulation on Th1/TH2 Cytokines Transcription at Materno-fetal Interface and Outcomes of Pregnancy

作　　者：朱晓勇[1] 李大金[1] 严缘昌[2] 

机构地区：[1]复旦大学妇产科研究所生殖免疫研究室,上海200011 [2]中国科学院上海生命科学研究院生物化学与细胞生物学研究所,上海200032

出　　处：《生殖与避孕》2004年第2期65-69,共5页Reproduction and Contraception

基　　金：国家自然基金(39770773);中国科学院上海细胞生物学研究所开放课题基(10-3303)金资助

摘　　要：目的探讨干预CD86协同刺激信号对母胎界面Th1/Th2型细胞因子转录调控及妊娠结局的影响。方法:将正常妊娠模型(CBA/J×BALB/c)和自然流产模型(CBA/J×DBA/2J)CBA孕鼠均分为两组:对照组(各10只)于孕d 4、d 6、d 8腹腔注射大鼠IgG;干预组(各10只)于孕d 4、d 6、d 8腹腔注射大鼠抗小鼠CD86 mAb。孕d 9竞争性半定量RT-PCR测定各组母胎界面组织中Th1型(IL-12、IFN-γ)/Th2型(IL-4、IL-10)细胞因子转录水平;孕d 12比较两种模型各组的胚胎吸收率。结果:正常妊娠模型中,干预CD86协同刺激信号对母胎界面Th1/Th2型细胞因子转录水平及妊娠预后均无显著影响(P>0.05)。自然流产模型中,干预CD86协同刺激信号能够升调节母胎界面局部Th2型而降调节Th1型细胞因子转录水平,并显著改善其妊娠预后(P<0.05)。结论:于孕早期干预CD86协同刺激信号能够调控母胎界面局部Th1/Th2型细胞因子转录,形成维持正常妊娠所需的Th2型免疫偏倚,诱导母胎免疫耐受。Objective: To study the influence of blockade of CD86 costimulation on Th1/Th2 cytokines transcriptional regulation at materno-fetal interface and the outcomes of pregnancy. Methods: Pregnant DBA/2J mated CBA/J mice with a high embryo resorption rate of 20% to 30% and BALB/c mated CBA/J mice with low embryo resorption rates were studied, with rat anti-murine CD86 mAb being administered intraperitoneally at the dosage of 100 mg, at day 4, 6, 8 of gestation. Competitive semiquantity RT-PCR was applied to analysis the transcription of Th1/Th2 cytokines at the maternal-fetal interface at day 9 of gestation, then the embryo resorption rate was counted at day 12 of gestation. Results: In the model of normal pregnancy, blockade of CD86 costimulation had no significant effects on the original Th2 bias at the materno-fetal interface, and the outcomes of gestation had not changed significantly (P>0.05). While in the model of abortion-prone, blockade of CD86 costimulation successfully induced a Th2 bias at materno-fetal interface at transcriptional level. Therefore, the embryo resorbing rates decreased significantly (P<0.05). Conclusion: Blockade of CD86 costimulation had a potent role in inducing Th2 bias at materno-fetal interface and rescuing the allogeneic fetus from rejection of maternal in a murine model.

关 键 词：协同刺激信号 CD86 母胎界面 TH1/TH2型细胞因子 

分 类 号：R714.21[医药卫生—妇产科学]