Fas ligand-induced apoptosis as a mechanism of immune privilege

Thomas S. Griffith, Thomas Brunner, Sharon M. Fletcher, Douglas R. Green, Thomas A. Ferguson

Research output: Contribution to journalArticlepeer-review

1893 Scopus citations

Abstract

The eye is a privileged site that cannot tolerate destructive inflammatory responses. Inflammatory cells entering the anterior chamber of the eye in response to viral infection underwent apoptosis that was dependent on Fas (CD95)-Fas ligand (FasL) and produced no tissue damage. In contrast, viral infection in gld mice, which lack functional FasL, resulted in an inflammation and invasion of ocular tissue without apoptosis. Fas-positive but not Fas-negative tumor cells were killed by apoptosis when placed within isolated anterior segments of the eyes of normal but not FasL-negative mice. FasL messenger RNA and protein were detectable in the eye. Thus, Fas-FasL interactions appear to be an important mechanism for the maintenance of immune privilege.

Original languageEnglish (US)
Pages (from-to)1189-1192
Number of pages4
JournalScience
Volume270
Issue number5239
StatePublished - Nov 17 1995
Externally publishedYes

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