摘要
目的 探讨协同刺激分子CD86在母 胎免疫调节中的作用。方法 建立自然流产模型(CBA×DBA/ 2 )及正常妊娠模型 (CBA×BALB/c)。两种模型分别再分为 3个组 :(1)以大鼠的IgG为对照的对照组 ;(2 )于妊娠第 4、6、8、10天 ,分别给CBA孕鼠腹腔注射大鼠抗小鼠CD86单克隆抗体的多次干预组 ;(3)仅于妊娠第 4天 ,给CBA孕鼠单次腹腔注射抗CD86单克隆抗体的单次干预组。每次腹腔注射的抗体剂量均为 10 0 μg。于妊娠第 14天计算各组胚胎吸收率。 结果 (1)自然流产模型与正常妊娠模型的对照组胚胎吸收率分别为 2 7 78%和 8 42 %。 (2 )于妊娠第 4、6、8、10天腹腔注射抗CD86单克隆抗体后 ,自然流产模型的多次干预组胚胎吸收率下降至 9 6 8% (P <0 0 5 ) ;而正常妊娠模型的多次干预组胚胎吸收率上升至 13 5 4% (P >0 0 5 )。 (3)妊娠第 4天单次腹腔注射抗CD86单克隆抗体 ,自然流产模型单次干预组的胚胎吸收率下降至 7 14% (P <0 0 0 1) ;而正常妊娠模型单次干预组的胚胎吸收率上升至 11 39% (P >0 0 5 )。结论 妊娠早期 ,尤其在胚胎对母体的致敏阶段 (着床期 ) ,阻断母 胎界面的CD86协同刺激信号 ,将诱导母体对胚胎的免疫耐受 ,从而减少胚胎吸收 。
Objective To evaluate the role of costimulating molecule CD86 in maternal fetal immune regulation. Methods In abortion prone (CBA×DBA/2) matings and non abortion prone (CBA×BALB/c) matings, the pregnant CBA females were injected intraperitoneally by purified rat anti murine CD86 monoclonal antibody (mAb) with dosage of 100 μg at day 4, 6, 8 and 10 of gestation respectively, or injected only once at day 4 of gestation, or injected with purified rat IgG as control. The resorbing and non resorbing embryos were enumerated at day 14 of gestation. Results The embryo resorbing rate in CBA×DBA/2 matings was 27 78%, and that in CBA×BALB/c matings was 8 42%. After injection of anti CD86 mAb at day 4, 6, 8, 10 of gestation, the embryo resorbing rate reduced to 9 68% ( P <0 005) in CBA×DBA/2 matings, while that was 13 54% in CBA×BALB/c matings ( P >0 05). After injection of anti CD86 mAb only once at day 4 of gestation, the embryo resorbing rate reduced apparently to 7 14% ( P <0 001) in CBA×DBA/2 matings, while that was 11 39% ( P >0 05) in CBA×BALB/c matings. Conclusions Blocking the costimulating signal by anti CD86 mAb at maternal fetal interface, especially at the prime stage of maternal fetal recognition (periods of implantation), may result in maternal fetal tolerance, and hopefully the embryo resorption turns to normal pregnancy.
出处
《中华妇产科杂志》
CAS
CSCD
北大核心
2001年第1期20-23,共4页
Chinese Journal of Obstetrics and Gynecology
基金
国家自然科学基金资助!(39770 773)