EXPRESSION OF THE APOPTOSIS-INDUCING FAS LIGAND (FASL) IN HUMAN FIRSTAND 3RD-TRIMESTER PLACENTA AND CHORIOCARCINOMA CELLS

Citation
Am. Bamberger et al., EXPRESSION OF THE APOPTOSIS-INDUCING FAS LIGAND (FASL) IN HUMAN FIRSTAND 3RD-TRIMESTER PLACENTA AND CHORIOCARCINOMA CELLS, The Journal of clinical endocrinology and metabolism, 82(9), 1997, pp. 3173-3175
Citations number
21
Categorie Soggetti
Endocrynology & Metabolism
ISSN journal
0021972X
Volume
82
Issue
9
Year of publication
1997
Pages
3173 - 3175
Database
ISI
SICI code
0021-972X(1997)82:9<3173:EOTAFL>2.0.ZU;2-P
Abstract
The Fas (Apo-1/CD95) ligand (Fast) belongs to the tumor necrosis facto r family and acts through its receptor (FasR/Apo-1/CD95) to induce apo ptosis in target cells. Fast is expressed in several immunologically p rivileged sites. Induction of apoptosis by Fast in invading lymphocyte s acts as a mechanism of immune privilege and is important in preventi ng graft rejection. Furthermore, Fast is expressed in certain malignan cies and it has been implicated as a possible key mechanism in immune privilege of these tumors. Since the invading placental trophoblast is another very important site with a privileged immune status, we inves tigated whether Fast is expressed in the normal and tumoral human plac enta. For this purpose, mRNA was extracted from first and third trimes ter human placental samples as well as from JEG3 choriocarcinoma cells and reverse transcribed to obtain cDNAs. These were used as templates for PCR analysis of Fast expression, in which specific primers were e mployed to amplify an 853 bp fragment spanning the whole Fast coding r egion. A product of the appropriate length was amplified from normal p lacenta as well as from the choriocarcinoma cells. Expression of Fast protein was confirmed by Western Blot and was localized to trophoblast by immunohistochemistry using a Fast-specific antibody. Expression of Fast in the human placenta indicates that induction of apoptosis in l ymphocytes by the invading trophoblast could be an important mechanism implicated in the immune tolerance of the fetal semi-allograft.