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.
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