Fas ligand-induced apoptosis as a mechanism of immune privilege.
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.
Griffith
T S
TS
Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, MO 63110, USA.
Brunner
T
T
Fletcher
S M
SM
Green
D R
DR
Ferguson
T A
TA
D000818:Animals; D000867:Anterior Chamber / Q000276:immunology* / Q000821:virology; D017209:Apoptosis; D001483:Base Sequence; D005123:Eye / Q000378:metabolism; D053222:Fas Ligand Protein; D015870:Gene Expression; D007108:Immune Tolerance; D016849:Keratitis, Herpetic / Q000276:immunology; D007939:Leukemia L1210; D008214:Lymphocytes / Q000166:cytology / Q000276:immunology; D008562:Membrane Glycoproteins / Q000032:analysis / Q000235:genetics / Q000502:physiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D008969:Molecular Sequence Data; D009504:Neutrophils / Q000166:cytology / Q000276:immunology; D012333:RNA, Messenger / Q000032:analysis / Q000235:genetics; D014407:Tumor Cells, Cultured; D019014:fas Receptor / Q000502:physiology
D053222:Fas Ligand Protein; C505658:Fasl protein, mouse; D008562:Membrane Glycoproteins; D012333:RNA, Messenger; D019014:fas Receptor