PASSIVE IMMUNIZATION FOR DEFINING FUNCTION OF PLACENTAL MHC CLASS I MOLECULES

这个子项目是许多利用资源的研究子项目之一 由NIH/NCRR资助的中心拨款提供。子项目的主要支持 子项目的主要研究者可能是由其他来源提供的， 包括其它NIH来源。 列出的子项目总成本可能 代表子项目使用的中心基础设施的估计数量， 而不是由NCRR赠款提供给子项目或子项目工作人员的直接资金。 目的：探讨MHC Ⅰ类分子在母胎界面表达的功能。 进展： 我们以前已经表明，被动免疫对胎盘特异性 MHC-I类分子Mamu-AG在妊娠第二周导致急性 （一周内）胎盘生长和发育中断， 分化和白细胞分布。为了了解长期的 由于这种效应，一只恒河猴在妊娠早期接受了以下治疗： 抗Mamu-AG，另一个用非特异性对照抗体处理。 允许妊娠进行至足月。在这项试点研究中，我们发现 妊娠期特异性和非特异性免疫 动物，比较早期胎儿生长受限，明显追赶胎儿生长， 胎盘血管化畸形，原代胎盘盘缺陷 生长伴随着继发性椎间盘代偿，以及胎儿 红细胞压积，可能是为了补偿早期的胎盘功能障碍。这些结果 这可能表明一个范例，有可能诱导早期胎盘 在整个妊娠期及以后具有后果的生长/功能损伤， 关于改变胎儿的结果。 出版物： 没有。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Objective: To identify the function of MHC class I expression at the maternal-fetal interface. PROGRESS: We have previously shown that passive immunization against the placenta-specific MHC class I molecule Mamu-AG in the second week of gestation results in an acute (within one week) disruption of placental growth and development, and decidual differentiation and leukocyte distribution. In order to understand the long-term consequences of this effect, one rhesus monkey was treated in early pregnancy with anti-Mamu-AG, and another was treated with a nonspecific control antibody. Pregnancies were allowed to proceed to term. In this pilot study, we identified differences between pregnancy in the specifically and nonspecifically immunized animals, comparing early fetal growth restriction, apparent catch-up fetal growth, placental dysmorphogenesis of vascularization, deficient primary placental disk growth accompanied by secondary disk compensation, and an increased fetal hematocrit, perhaps in compensation for earlier placental dysfunction. These results may indicate a paradigm which has the potential to induce an early placental growth/function insult which has consequences throughout gestation and beyond, with regards to altered fetal outcomes. PUBLICATIONS: None.