FAS LIGAND-INDUCED APOPTOSIS AS A MECHANISM OF IMMUNE PRIVILEGE

Citation
Ts. Griffith et al., FAS LIGAND-INDUCED APOPTOSIS AS A MECHANISM OF IMMUNE PRIVILEGE, Science, 270(5239), 1995, pp. 1189-1192
Citations number
26
Categorie Soggetti
Multidisciplinary Sciences
Journal title
ISSN journal
00368075
Volume
270
Issue
5239
Year of publication
1995
Pages
1189 - 1192
Database
ISI
SICI code
0036-8075(1995)270:5239<1189:FLAAAM>2.0.ZU;2-E
Abstract
The eye is a privileged site that cannot tolerate destructive inflamma tory responses. inflammatory cells entering the anterior chamber of th e eye in response to viral infection underwent apoptosis that was depe ndent on Fas (CD95)-Fas ligand (FasL) and produced no tissue damage. I n contrast, viral infection in gld mice, which lack functional Fast, r esulted in an inflammation and invasion of ocular tissue without apopt osis. Fas-positive but not Fas-negative tumor cells were killed by apo ptosis when placed within isolated anterior segments of the eyes of no rmal but not Fast-negative mice. Fast messenger RNA and protein were d etectable in the eye. Thus, Fas-FasL interactions appear to be:an impo rtant mechanism for the maintenance of immune privilege.