RT Journal Article
SR Electronic
T1 Fas Ligand-Induced Apoptosis as a Mechanism of Immune Privilege
JF Science
JO Science
FD American Association for the Advancement of Science
SP 1189
OP 1192
DO 10.1126/science.270.5239.1189
VO 270
IS 5239
A1 Griffith, Thomas S.
A1 Brunner, Thomas
A1 Fletcher, Sharon M.
A1 Green, Douglas R.
A1 Ferguson, Thomas A.
YR 1995
UL http://science.sciencemag.org/content/270/5239/1189.abstract
AB 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.