Fas-fas ligand system-induced apoptosis in human placenta and gestational trophoblastic disease

Am J Reprod Immunol. 1998 Aug;40(2):89-94. doi: 10.1111/j.1600-0897.1998.tb00396.x.

Abstract

Problem: The low frequency of maternal immune responses to paternally inherited fetal antigens raises the following question: What regulates the immunobiology of pregnancy? Data suggest that this state is the result of peripheral immune-tolerance, an active process of immune-regulation in which activated T cells undergo apoptosis. We studied Fas ligand (FasL) expression and apoptosis in normal and pathologic placentas to find out whether the Fas-FasL-induced apoptosis takes place during implantation.

Method of study: FasL expression in paraffin sections was detected using specific antibodies and confirmed with reverse transcriptase-polymerase chain reaction of total RNA from frozen placentas. Apoptosis was detected using the terminal deoxy (d)-UTP nick end-labeling assay.

Results: FasL was found in the normal placenta and in gestational trophoblastic disease. Apoptotic leukocytes were localized to the maternal-fetal interface corresponding in localization with the distribution of FasL.

Conclusions: We propose that FasL expression in the placenta is a mechanism responsible for the development of maternal immune tolerance specific for paternal alloantigens and operates in pathologic states characterized by trophoblastic invasion/proliferation.

MeSH terms

  • Apoptosis*
  • Choriocarcinoma / immunology
  • Fas Ligand Protein
  • Female
  • Fetus / immunology
  • Humans
  • Hydatidiform Mole / immunology
  • Immunohistochemistry
  • Membrane Glycoproteins / genetics
  • Membrane Glycoproteins / metabolism*
  • Placenta / immunology*
  • Polymerase Chain Reaction
  • Pregnancy / immunology*
  • Pregnancy Trimester, First / immunology
  • Pregnancy Trimester, Third / immunology
  • Trophoblasts / immunology
  • Uterine Neoplasms / immunology
  • fas Receptor / genetics
  • fas Receptor / metabolism*

Substances

  • FASLG protein, human
  • Fas Ligand Protein
  • Membrane Glycoproteins
  • fas Receptor