Maternal-fetal Immune Interactions Research Articles

Recent developments in the human maternal-fetal immune interaction

This review discusses the three important developments that are likely to have the greatest impact on our understanding of human reproductive immunology: the establishment of the trophoblast major histocompatibility complex class I antigen as HLA-G; the identification of the trophoblast-lymphocyte-crossreactive protein as a complement regulatory protein; and elucidation of the lineage and possible functions of decidual large granular lymphocytes.

Major histocompatibility antigens on trophoblast and their regulation: implications in the maternal-fetal relationship.

Recent technological advances have provided methods of detecting antigens encoded by the major histocompatibility complex with greater precision, allowing the expression of such antigens on the components of the placenta to be clarified. Of specific interest is the expression of these antigens on trophoblast cells, the fetal-derived epithelial cells that confront maternal blood and tissues at the maternal-fetal interface. It is now clear that the different trophoblast subpopulations differentially express class I antigens, although none appear to express class II antigens. Class I antigens can be induced by exposure to interferons on some populations but apparently not others, suggesting that the regulation of their expression differs for subpopulations of trophoblast cells, depending on gestational stage and location. This restricted expression has important implications for maternal-fetal immune interactions during the different phases of pregnancy and perhaps also bears on physiological functions of the feto-placental unit, such as growth and differentiation.

Maternal—fetal immune interactions and the maintenance of major histocompatibility complex polymorphism in the rat

In several different strain combinations of rats, an R 2 backcross was used to assess the relative fitness of progeny MHC-incompatible with their mothers as compared to that of MHC-compatible progeny. None of the various treatments used to alter maternal immunoregulatory processes, namely splenectomy, active or adoptive immunization, or the induction of transplantation tolerance, was able to perturb consistently the population distribution of RT1 antigens. Though the extreme variability of RT1 heterozygote excess remains poorly understood, studies of parity-associated changes in the population distribution of RT1 heterozygotes: RT1 homozygotes nonetheless do support the hypothesis that the spleen is important to the immunoregulatory control of these phenomena.