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The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

Fas Ligand-Induced Apoptosis as a Mechanism of Immune Privilege

Open access
Griffith, Thomas S., Brunner, Thomas, Fletcher, Sharon M., Green, Douglas R., Ferguson, Thomas A.·1995·Science

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.

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Crossref · 10.1126/science.270.5239.1189

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Metadata

Authors
Griffith, T. S., Brunner, T., Fletcher, S. M., Green, D. R., & Ferguson, T. A.
Venue
Science
Published
1995-11-17
Volume
270
Issue
5239
Pages
1189-1192
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
OpenAlex
W1978018492
Cited by
2,005
References
1
FWCI
42.28
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Fas Ligand-Induced Apoptosis as a Mechanism of Immune Privilege. https://app.cochat.ai/papers/10.1126/science.270.5239.1189
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Griffith, T. S., Brunner, T., Fletcher, S. M., Green, D. R., & Ferguson, T. A. (1995). Fas Ligand-Induced Apoptosis as a Mechanism of Immune Privilege. Science. https://doi.org/10.1126/science.270.5239.1189

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