Abstract:
:During mammalian pregnancy, one or more semiallogeneic fetuses gestate in direct contact with the maternal circulation and uterine tissue. However, a damaging maternal immune response is not normally provoked. We studied two possible mechanisms for this maternal-fetal tolerance, alone and in combination. First, we directly tested the hypothesis that the striking absence of MHC class I molecules on most placenta trophoblasts protects the fetus from maternal immune attack, by creating transgenic mice which express Ld in giant cell trophoblasts. Second, because Fas ligand (FasL) may contribute to immune privilege, we tested whether functional FasL expression by the fetus, or Fas expression by the mother, contributes to successful reproduction in a fully allogeneic breeding. Our data indicate that neither abnormal expression of MHC class I in giant cells, nor disruption of the Fas-FasL system, nor a combination of these two defects, has an adverse effect on pregnancy outcome. These results suggest that during healthy allogeneic pregnancy, down-regulation of MHC class I and expression of FasL on placenta are not critical events, and other factors must prevent a harmful maternal immune response.
journal_name
Eur J Immunoljournal_title
European journal of immunologyauthors
Rogers AM,Boime I,Connolly J,Cook JR,Russell JHdoi
10.1002/(SICI)1521-4141(199811)28:11<3479::AID-IMMsubject
Has Abstractpub_date
1998-11-01 00:00:00pages
3479-87issue
11eissn
0014-2980issn
1521-4141journal_volume
28pub_type
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