Trophoblasts express Fas ligand: a proposed mechanism for immune privilege in placenta and maternal invasion
Abstract
Cross-linking of Fas (CD95, APO-1) and Fas ligand (FasL; CD95L) induces apoptosis of Fas-bearing cells. Recent evidence suggests that FasL. expression plays an important role in maintenance of immune privilege in murine testis and eye and in tumour escape from immune rejection in colon cancer, melanoma and hepatocellular carcinoma. Bcl-2 is a membrane protein that suppresses apoptosis in response to a variety of stimuli. In this paper we describe abundant expression of FasL protein and mRNA transcripts within the immune privileged environment of the placenta by immunohistochemistry and reverse transcription in-situ polymerase chain reaction methods. The syncytiotrophoblast layer, the main site of feto-maternal interface, and extravillous trophoblasts, demonstrated consistent immunoreactivity for FasL in term placentae. Co-occurrence of Fas and Bcl-2 were detected with a similar pattern of distribution with FasL. The TUNEL method revealed evidence of apoptosis in the placental tissues. We speculate that abundant presence of FasL in the trophoblast contributes to immune privilege in this unique environment, perhaps by fostering apoptosis of activated Fas-expressing lymphocytes of maternal origin. An apoptotic process mediated by FasL may also play a role in placental invasion during implantation and underscores similarities between the trophoblast and neoplastic cells.
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Some studies concluded that complications during pregnancy and foetal death in P. falciparum placental malaria might be determined by changes in the regulation of apoptosis via Fas/FasL and increased Th1 immune responses in the syncytiotrophoblast.
“Some studies concluded that complications during pregnancy and foetal death observed in P. falciparum placental malaria might be determined by changes in the regulation of apoptosis, via Fas /FasL [9], and increased Th1 immune responses in the syncytiotrophoblast [10,11].”
From Submicroscopic infection of placenta by Plasmodium produces Th1/Th2 cytokine imbalance, inflammation and hypoxia in women from north-west Colombia (2014) · cites this paper as [9]
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- Authors
- Uckan, D.
- Venue
- Molecular Human Reproduction
- Publisher
- Oxford University Press (OUP)
- Published
- 1997-08-01
- Volume
- 3
- Issue
- 8
- Pages
- 655-662
- ISSN
- 1360-9947 (ISSN-L)
- 1460-2407
- OpenAlex
- W2104330540
- Cited by
- 206
- References
- 46
- Citations by year
- 2026: 3 · 2025: 1 · 2024: 3 · 2023: 3 · 2022: 3 · 2021: 5 · 2020: 3 · 2019: 3 · 2018: 3 · 2017: 6 · 2016: 1 · 2015: 5 · 2014: 5 · 2013: 2 · 2012: 5
- FWCI
- 5.38
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Molecular Human Reproduction (publishedVersion)
- PubMed (publishedVersion)
- Funders
- McMaster University
- U.S. Public Health Service (05628-13)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Reproductive System and Pregnancy
- Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- Fas ligand, trophoblast, immune privilege, placenta, syncytiotrophoblast, extravillous trophoblast, Bcl-2, apoptosis, maternal-fetal interface, maternal-fetal immune tolerance, implantation, tumor immune evasion
- MeSH terms
- Female, Humans, Membrane Glycoproteins, Placenta, Pregnancy, RNA, Messenger, Transcription, Genetic, Trophoblasts, Polymerase Chain Reaction, Apoptosis, fas Receptor, Fas Ligand Protein
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