Fetoplacental physiology in relation to metabolic diseases

  • W . Page Faulk
  • Published 1984 in Journal of Inherited Metabolic Disease


The placenta and amniochorion which interface with maternal cells are products of embryonic and not maternal genes, and their coexistence as allogeneic tissues might have been expected to summon the already well-developed immunological system to reject, and thus disallow, the implantation of a fertile egg or blastocyst within the maternal uterus. Instead, the primordial uterus not only accepted this intruder, but developed ways and means to nourish it through a nine month gestation. This simple fact lies at the basis of much contemporary enthusiasm for pregnancy research. Most medical people tend to imagine the existence of a materno-fetal relationship that is governed primarily by the placenta, but both of these concepts are anatomically incorrect. There are no interfaces of contact between maternal and embryonic or fetal tissue. The fetal contribution is entirely extra-embryonic, and the extra-embryonic tissue which is presented to maternal cells at all of these interfaces is the trophoblast. Thus, the materno-fetal relationship does not exist directly but only in a functional sense at the molecular level, but there is such a thing as the maternotrophoblastic relationship, and this phrase should be used and distinguished from the materno-fetat relationship. Mothers produce antibodies to placental polysaccharides (Kaku, 1953; Levanon and Rossetini, 1968) and to fractions of solubilized placental microsomes (Gaugas and Curzen, 1979). Various pot-pourri of placental antigens have also been used to show cellmediated immune reactions to placental antigens during a first pregnancy. Taylor and Hancock (1975) developed an in vitro procedure which allowed them to show that maternal leukocytes were capable of producing a trophoblastotoxic effect which could be blocked by something in maternal blood. Technology has been an impediment in this field of research, but recently Davies and Sutcliffe (1982) and Davies et al. (1982a, b) have proposed what appears to be a promising technological advance for the detection of both humoral and cellular immune responses to trophoblast. Some aborting women have very high titred cytotoxic antibodies which are often specific for their husbands' lymphocytes (Faulk and McIntyre, 1983). These women have obviously been immunologically stimulated, so why do they abort? The response to this lies in the nature of their antibodies. In the first instance, these

DOI: 10.1007/BF01805605

Cite this paper

@article{Faulk1984FetoplacentalPI, title={Fetoplacental physiology in relation to metabolic diseases}, author={W . Page Faulk}, journal={Journal of Inherited Metabolic Disease}, year={1984}, volume={7}, pages={172-174} }