@article{Lin1998ligan-14307,
  year={1998},
  doi={10.1172/JCI896},
  title={Fas ligand-mediated killing by intestinal intraepithelial lymphocytes : Participation in intestinal graft-versus-host disease},
  number={3},
  volume={101},
  issn={0021-9738},
  journal={The journal of clinical investigation : JCI},
  pages={570--577},
  author={Lin, Tesu and Brunner, Thomas and Tietz, Brian and Madsen, Jill and Bonfoco, Emanuela and Reaves, Miriam and Huflejt, Margaret and Green, Douglas R.}
}

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    <dc:creator>Brunner, Thomas</dc:creator>
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    <dc:contributor>Brunner, Thomas</dc:contributor>
    <dcterms:title>Fas ligand-mediated killing by intestinal intraepithelial lymphocytes : Participation in intestinal graft-versus-host disease</dcterms:title>
    <dc:contributor>Tietz, Brian</dc:contributor>
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    <dc:creator>Huflejt, Margaret</dc:creator>
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    <dcterms:issued>1998</dcterms:issued>
    <dc:language>eng</dc:language>
    <dc:contributor>Lin, Tesu</dc:contributor>
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    <dc:creator>Bonfoco, Emanuela</dc:creator>
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    <dcterms:bibliographicCitation>First publ. in: The journal of clinical investigation : JCI ; 101 (1998), 3. - S. 570-577</dcterms:bibliographicCitation>
    <dc:contributor>Madsen, Jill</dc:contributor>
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    <dc:date rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2011-07-29T08:30:11Z</dc:date>
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    <dc:creator>Tietz, Brian</dc:creator>
    <dc:creator>Reaves, Miriam</dc:creator>
    <dc:creator>Madsen, Jill</dc:creator>
    <dc:contributor>Huflejt, Margaret</dc:contributor>
    <dc:contributor>Reaves, Miriam</dc:contributor>
    <dcterms:abstract>In vitro studies have demonstrated that intestinal intraepithelial lymphocytes (IEL) are constitutively cytotoxic; however, the mechanism and target of their cytotoxicity are unknown. Apoptosis of intestinal epithelial cells (IEC) and an increase in IEL numbers are classical signs of intestinal graft-versus-host disease (GVHD), although whether IEL can mediate IEC apoptosis directly in GVHD is unclear. Recent evidence suggests that target epithelial organ injury observed in GVHD is predominantly Fas-mediated; therefore, we investigated the possibility that IEL induce apoptosis of IEC through a Fas-mediated mechanism. Here, we demonstrate that the IEL isolated from normal mice readily display potent Fas ligand (FasL)-mediated killing activity after CD3 stimulation, and that IEC express Fas, suggesting that IEC are potential targets for FasL-mediated killing by IEL. In vitro, IEL isolated from GVHD mice have markedly increased FasL-mediated killing potential and are spontaneously cytolytic toward host-derived tumor cells predominantly through a Fas-mediated pathway. In vivo transfer of IEL isolated from GVHD mice induced significantly more IEC apoptosis in F1 wild-type mice than in Fas-defective F1lpr mice. Thus, these results demonstrate that FasL-mediated death of IEC by IEL is a major mechanism of IEC apoptosis seen in GVHD.</dcterms:abstract>
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    <dc:creator>Green, Douglas R.</dc:creator>
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    <dc:contributor>Bonfoco, Emanuela</dc:contributor>
    <dc:creator>Lin, Tesu</dc:creator>
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