PASSIVE IMMUNIZATION FOR DEFINING FUNCTION OF PLACENTAL MHC CLASS I MOLECULES

这个子项目是利用资源的许多研究子项目之一。 由NIH/NCRR资助的中心拨款提供。对子项目的主要支持 子项目的首席调查员可能是由其他来源提供的， 包括美国国立卫生研究院的其他来源。为子项目列出的总成本可能 表示该子项目使用的中心基础设施的估计数量， 不是由NCRR赠款提供给次级项目或次级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。 进度： 我们之前已经证明，针对胎盘特异性的被动免疫 MHC-I类分子MAMU-AG在妊娠第二周导致急性 (一周内)胎盘生长发育受阻和蜕膜 分化和白细胞分布。为了了解长期的 这种影响的后果是，一只恒河猴在怀孕早期接受了 抗MAMU-AG，另一组用非特异性对照抗体处理。 怀孕被允许继续到足月。在这项初步研究中，我们发现 特异性免疫者与非特异性免疫者妊娠的差异 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，原发胎盘缺陷 伴随着发育的二次盘代偿，以及胎儿 红细胞压积，可能是对早期胎盘功能障碍的补偿。这些结果 可能表明一种有可能诱导早期胎盘发育的范例 发育/功能侮辱，在整个怀孕期间及以后都会产生影响， 关于胎儿结局的改变。 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.