Species diversity in the immunogenetic relationship between mother and fetus: is trophoblast insusceptibility to immunological destruction the only essential common feature for the maintenance of allogeneic pregnancy?
Maternal-fetal immune interactions in pregnancy have been examined in a number of different species using a wide range of experimental procedures, many of which have been incapable of providing information on the specificity of the immunological parameters measured. As a result, data have often been unconvincing, unsubstantiated or conflicting. It is clear that considerable species diversity exists in the precise nature of the maternal immune responses elicited against the genetically dissimilar fetus. These may, however, be an irrelevant consequence of fetomaternal genetic incompatibilities. A feature common to all eutherian mammalian species, that could alone be responsible for the maintenance of allogeneic pregnancy, is the apparent insusceptibility of the fetal trophoblast to immune destruction. This is effected in some species by an absence of appropriate target molecules, particularly classical class I MHC antigens, on the trophoblast cell surface, and in others possessing these (and possibly other) target structures, by the local trophoblastic secretion of soluble factors, not yet fully characterised, that appear to be capable of inhibiting binding and interaction with cells of the maternal immune system. As there is no convincing evidence for transplacental transfer of significant numbers of maternal lymphocytes, the survival of the allogeneic fetus is likely to be ensured by the impenetrability of the trophoblastic tissue barrier and its resistance to maternal immunologically mediated attack. Should this be firmly established, it would not be necessary to invoke any of the immunoregulatory mechanisms that have been claimed to be essential for successful implantation and development of the mammalian embryo. This would in turn negate the concept of an alloimmune aetiology for pregnancy failure and hence also the rationale for those therapeutic procedures intended to restore the assumed inadequate maternal alloimmune protective responses.
Billington
W D
WD
Department of Pathology and Microbiology, School of Medical Sciences, University of Bristol, UK.
D000818:Animals; D005260:Female; D005333:Fetus / Q000276:immunology*; D006680:HLA Antigens / Q000276:immunology; D059951:HLA-G Antigens; D015395:Histocompatibility Antigens Class I / Q000276:immunology; D007108:Immune Tolerance; D007518:Isoantibodies / Q000096:biosynthesis / Q000276:immunology; D008431:Maternal-Fetal Exchange / Q000276:immunology*; D051379:Mice / Q000196:embryology / Q000276:immunology; D011247:Pregnancy / Q000276:immunology*; D011270:Pregnancy, Animal / Q000276:immunology*; D051381:Rats / Q000196:embryology / Q000276:immunology; D013045:Species Specificity; D014327:Trophoblasts / Q000276:immunology*; D015017:Yolk Sac / Q000276:immunology
D006680:HLA Antigens; D059951:HLA-G Antigens; D015395:Histocompatibility Antigens Class I; D007518:Isoantibodies