FAS LIGAND-INDUCED APOPTOSIS AS A MECHANISM OF IMMUNE PRIVILEGE

被引:1748
作者
GRIFFITH, TS
BRUNNER, T
FLETCHER, SM
GREEN, DR
FERGUSON, TA
机构
[1] WASHINGTON UNIV, SCH MED, DEPT OPHTHALMOL & VISUAL SCI, ST LOUIS, MO 63110 USA
[2] WASHINGTON UNIV, SCH MED, DEPT PATHOL, ST LOUIS, MO 63110 USA
[3] LA JOLLA INST ALLERGY & IMMUNOL, DIV CELLULAR IMMUNOL, LA JOLLA, CA 92037 USA
关键词
D O I
10.1126/science.270.5239.1189
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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 Fast, 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 Fast-negative mice. Fast 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.
引用
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页码:1189 / 1192
页数:4
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