Fas ligand-induced apoptosis as a mechanism of immune privilege

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

Fas ligand-induced apoptosis as a mechanism of immune privilege

Dateien

1995_Griffith_Fas Ligand.pdf(2.3 MB)

Datum

1995

Autor:innen

Griffith, Thomas S.

Brunner, Thomas

Fletcher, Sharon M.

Green, Douglas R.

Ferguson, Thomas A.

Publikationstyp

Zeitschriftenartikel

Erschienen in

Science ; 270 (1995), 5239. - S. 1189-1192. - ISSN 0036-8075

Zusammenfassung

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.

Fachgebiet (DDC)

570 Biowissenschaften, Biologie

Zitieren

ISO 690

GRIFFITH, Thomas S., Thomas BRUNNER, Sharon M. FLETCHER, Douglas R. GREEN, Thomas A. FERGUSON, 1995. Fas ligand-induced apoptosis as a mechanism of immune privilege. In: Science. 270(5239), pp. 1189-1192. ISSN 0036-8075. Available under: doi: 10.1126/science.270.5239.1189

BibTex

@article{Griffith1995ligan-14318,
  year={1995},
  doi={10.1126/science.270.5239.1189},
  title={Fas ligand-induced apoptosis as a mechanism of immune privilege},
  number={5239},
  volume={270},
  issn={0036-8075},
  journal={Science},
  pages={1189--1192},
  author={Griffith, Thomas S. and Brunner, Thomas and Fletcher, Sharon M. and Green, Douglas R. and Ferguson, Thomas A.}
}

RDF

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