Fas ligand- mediated killing by intestinal intraepithelial lymphocytes. Participation in intestinal graft-versus-host disease.

Lin, Tiejun; Brunner, Thomas; Tietz, Brian; Madsen, Jill; Bonfoco, Emanuela; Reaves, Miriam; Huflejt, Margaret E.; Green, Douglas R.

doi:10.1172/jci896

Cited by 122 publications

(88 citation statements)

References 36 publications

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“…Quantitative measurements were performed in triplicate and standardized to the internal control of ␤-actin mRNA for each sample. Functionality of IEC FasL was analyzed by killing of L1210-and L1210-Fas target cells as described (19).…”

Section: Methodsmentioning

confidence: 99%

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Nonlymphoid Fas ligand in peptide-induced peripheral lymphocyte deletion

Pinkoski

Droin²,

Lin³

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

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Section: Methodsmentioning

confidence: 99%

“…OT-2 transgenic mice were assessed by three-color analysis with anti-CD4-CyChrome, anti-V␣2-phycoerythrin, and anti-V␤8-FITC. Lymphocytes were isolated from spleens and lymph nodes, and primary intestinal epithelial cells (IECs) were isolated as outlined (19).…”

mentioning

confidence: 99%

Nonlymphoid Fas ligand in peptide-induced peripheral lymphocyte deletion

Pinkoski

Droin²,

Lin³

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

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“…Because SEB induces the expression of FasL on T cells (43), it is possible that apoptosis of epithelial cells was mediated by interactions between Fas and FasL. This model is supported by the results of other studies documenting the expression of Fas on epithelial cells and FasL by intestinal T cells in graft-vs-host disease (54,55). Previous reports have suggested that changes in epithelial cell structure and function can occur after exposing tissue to SEB (41,56).…”

Section: Figurementioning

confidence: 70%

Staphylococcal Enterotoxin B Stimulates Expansion of Autoreactive T Cells That Induce Apoptosis in Intestinal Epithelial Cells: Regulation of Autoreactive Responses by IL-10

Ito

Takaishi

Jin

et al. 2000

The Journal of Immunology

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T cell responses to self Ags and normal microbial flora are carefully regulated to prevent autoreactivity. Because IL-10-deficient mice develop colitis, and this response is triggered by luminal flora, we investigated whether IL-10 regulates the ability of microbial Ags to induce autoreactive T cells that could contribute to intestinal inflammation. T cells from wild-type mice were primed with staphylococcal enterotoxin B (SEB) in vitro, which induced an autoreactive proliferative response to syngeneic feeder cells. The cells were predominately CD3+ and CD4+. T cells from IL-10-deficient mice were constitutively autoreactive, and SEB priming enhanced this further. The autoreactive, proliferative response of T cells from wild-type mice was suppressed by IL-10 in the primary or secondary culture, and this effect was inhibited by neutralizing Abs to the IL-10R. To confirm that an autoreactive repertoire was expanded after SEB priming, we used CBA/J mice (Mls-1a) in which autoreactive T cells recognizing the endogenous viral superantigen are depleted (Vβ6, 7, 8.1 TCR-bearing cells). However, SEB rescued these autoreactive T cell repertoires. Adding anti-MHC class II Ab blocked the autoreactive response. SEB-primed splenic or colonic T cells also induced apoptosis in syngeneic intestinal epithelial cells that was blocked significantly by IL-10. Thus, microbial Ags have the potential to abrogate self tolerance by stimulating autoreactive T cells that become cytolytic to target cells. IL-10 plays a protective role in maintaining self tolerance after microbial stimulation by preventing the activation of T cells that contribute to epithelial cell damage.

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“…Four mm paran-embedded sections were then stained with both Hematoxylin and Eosin (H&E) or with TUNEL (TdTmediated dUTP-biotin nick end labeling) staining as previously described (Lin et al, 1998).…”

Section: Histologymentioning

confidence: 99%

p53-dependent radiation-induced crypt intestinal epithelial cells apoptosis is mediated in part through TNF-TNFR1 system

et al. 2001

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Radiation induces apoptosis of crypt intestinal epithelial cells (IEC) through a pathway that is largely dependent on p53. However, exactly how p53 mediates IEC apoptosis is unclear. Studies in vitro suggest that one mechanism by which p53 mediates apoptosis is through its ability to transactivate members of the TNF receptor family of`Death Receptors'. Here, we examined the role of one of its member, TNF receptor type 1 (TNFR1), in an in vivo model of p53-dependent radiation-induced IEC apoptosis. We demonstrate that mice genetically engineered to be de®cient in TNF receptor type 1 (TNFR1 7/7) and mice injected with TNFR1-fusion chimeric protein (TNFR1-Fc; a competitive inhibitor of TNFR1) were partially protected (30 ± 40%) from p53-dependent radiation-induced IEC apoptosis. However, we found no evidence to support the possibility p53 transcriptionally regulates the expression of TNFR1 nor increases the susceptibility of IEC to TNF-mediated apoptosis. Interestingly, we found that injection of TNF readily induced IEC apoptosis and that radiation induced a p53-dependent increase in the intestinal level of TNF. Furthermore, injection of a neutralizing anti-TNF mAb reduced p53-dependent radiation-induced IEC apoptosis by approximately 60%. Overall, these results suggest that p53-dependent radiation-induced IEC apoptosis is mediated in part through ability of p53 to regulate TNF, which subsequently induces IEC apoptosis through TNFR1. Oncogene (2001) 20, 812 ± 818.

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Fas ligand- mediated killing by intestinal intraepithelial lymphocytes. Participation in intestinal graft-versus-host disease.

Cited by 122 publications

References 36 publications

Nonlymphoid Fas ligand in peptide-induced peripheral lymphocyte deletion

Nonlymphoid Fas ligand in peptide-induced peripheral lymphocyte deletion

Staphylococcal Enterotoxin B Stimulates Expansion of Autoreactive T Cells That Induce Apoptosis in Intestinal Epithelial Cells: Regulation of Autoreactive Responses by IL-10

p53-dependent radiation-induced crypt intestinal epithelial cells apoptosis is mediated in part through TNF-TNFR1 system

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