Fetal growth restriction is associated with reduced FasL expression by decidual cells.
The Fas-Fas ligand (FasL) system contributes to immune tolerance at the feto-maternal site and has been ascribed a role in implantation and placental development by regulating trophoblast invasion and spiral artery remodelling. In the present study, we have examined FasL expression in decidual tissue from pregnancies with impaired placental development. Women with pre-eclampsia (PE) and/or fetal growth restriction (FGR) were enrolled as cases (n=33), and women with normal pregnancies were used as controls (n=27). Decidua basalis tissue was obtained by vacuum suction of the placental bed after delivery. FasL expression by extravillous trophoblasts (EVTs) and decidual cells (DeCs), together with EVT apoptosis, were assessed by immunohistochemistry. Levels of soluble FasL in maternal serum and apoptosis-related gene expression in decidual tissue were determined. The proportion of FasL-expressing DeCs was high in controls (72.0+/-10.2%), with a significant reduction among cases (58.1+/-19.7%; p=0.002), especially in those with FGR (54.3+/-19.9%; p<0.001). EVTs had a lower proportion of FasL expression than DeCs, with a less pronounced reduction in cases compared to controls (10.9+/-3.9 and 8.3+/-4.0%, respectively; p=0.02). Decidual FasL expression correlated with placental growth. The EVT apoptosis rate did not differ between cases and controls (1.1+/-1.9 and 1.1+/-1.3%, respectively). These findings indicate a reduction of immune privilege in decidua of PE/FGR pregnancies by reduced FasL expression and that DeCs may have a central role in the Fas-FasL-based feto-maternal immune balance.
Eide
Irina P
IP
Department of Cancer Research and Molecular Medicine, DMF, Norwegian University of Science and Technology (NTNU), Medisinsk teknisk forskningssenter, Olav Kyrres gt. 3, N-7489 Trondheim, Norway. irina.p.eide@ntnu.no
Isaksen
Christina V
CV
Salvesen
Kjell A
KA
Langaas
Mette
M
Günther
Clara-Cecilie
CC
Iversen
Ann-Charlotte
AC
Austgulen
Rigmor
R
D017209:Apoptosis; D003656:Decidua / Q000166:cytology / Q000378:metabolism*; D053222:Fas Ligand Protein / Q000097:blood / Q000378:metabolism*; D005260:Female; D005317:Fetal Growth Retardation / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D015870:Gene Expression; D006801:Humans; D007108:Immune Tolerance; D007150:Immunohistochemistry; D009929:Organ Size; D010920:Placenta / Q000473:pathology; D010929:Placentation / Q000276:immunology; D011225:Pre-Eclampsia / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D011247:Pregnancy; D014327:Trophoblasts / Q000166:cytology / Q000378:metabolism
D053222:Fas Ligand Protein