Bonney Elizabeth A
Department of Obstetrics and Gynecology, University of Vermont College of Medicine, Given Building, Room C-244, 89 Beaumont Avenue, Burlington, VT 05405, USA.
J Reprod Immunol. 2007 Dec;76(1-2):68-74. doi: 10.1016/j.jri.2007.03.006. Epub 2007 May 4.
Classical thinking suggests that the immune system undergoes activation on the basis of discrimination between 'self' and 'non-self'. Accordingly, the fetus activates the mother's immune system because the fetus is in part 'non-self'. Thus, successful pregnancy depends on constraint of maternal immunity. Preeclampsia is an outcome of lost constraint. Instead, the danger model suggests that normal pregnancy, regardless of the expression of 'non-self' antigens, does not activate the maternal immune system unless that pregnancy expresses danger signals. Thus, preeclampsia stems from stress or abnormal cell death in pregnancy-related tissues. This compels expression of specific danger signals and potential activation of anti-fetal immunity, which secondarily feeds the syndrome. Study of preeclampsia from this perspective may bring forth novel mechanisms and indicators of vascular and metabolic dysfunction during pregnancy.
传统观点认为，免疫系统基于对“自身”和“非自身”的区分而被激活。因此，胎儿会激活母亲的免疫系统，因为胎儿部分属于“非自身”。所以，成功妊娠依赖于母体免疫的抑制。子痫前期是免疫抑制丧失的结果。相反，危险模型认为，正常妊娠无论“非自身”抗原的表达情况如何，除非妊娠表达危险信号，否则不会激活母体免疫系统。因此，子痫前期源于妊娠相关组织的应激或异常细胞死亡。这促使特定危险信号的表达以及抗胎儿免疫的潜在激活，进而引发该综合征。从这一角度研究子痫前期可能会揭示妊娠期间血管和代谢功能障碍的新机制及指标。
