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Expression of TRAIL receptors in human autoreactive and foreign antigen-specific T cells

Deletion of T cells due to apoptosis induction is a regulatory mechanism in the human immune system that may be impaired in autoimmune diseases such as multiple sclerosis (MS). Involvement of the apoptosis-mediating CD95/CD95 ligand system in MS has been demonstrated. Here, we report that (auto)anti...

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Bibliographic Details
Main Authors: Wendling, Uwe (Author) , Walczak, Henning (Author) , Krammer, Peter H. (Author)
Format: Article (Journal)
Language:English
Published: 27 June 2000
In: Cell death and differentiation
Year: 2000, Volume: 7, Issue: 7, Pages: 637-644
ISSN:1476-5403
DOI:10.1038/sj.cdd.4400692
Online Access:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1038/sj.cdd.4400692
Verlag, lizenzpflichtig, Volltext: https://www.nature.com/articles/4400692
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Author Notes:U. Wendling, H. Walczak, J. Dörr, C. Jaboci, M. Weller, P.H. Krammer and F. Zipp
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Summary:Deletion of T cells due to apoptosis induction is a regulatory mechanism in the human immune system that may be impaired in autoimmune diseases such as multiple sclerosis (MS). Involvement of the apoptosis-mediating CD95/CD95 ligand system in MS has been demonstrated. Here, we report that (auto)antigen-specific human T cells are not killed in vitro by soluble TNF-related apoptosis-inducing ligand (TRAIL) although expressing death-inducing receptors, TRAIL receptor 1 (TRAIL-R1) and TRAIL-R2. Apoptosis was assessed by caspase activation and DNA fragmentation, receptor expression was detected by RT-PCR and flow cytometry. The (auto)antigen-specific T cells were also resistant to specific TRAIL-R1/TRAIL-R2-directed induction of apoptosis, indicating that coexpression of the truncated TRAIL-R3 and TRAIL-R4 in these T cells is not responsible for the observed resistance. Upon stimulation, levels of death-inducing TRAIL receptors decreased whereas TRAIL was up-regulated on the cell surface. In contrast to CD95, the role of TRAIL receptors in MS might not involve regulation of T cell vulnerability.
Item Description:Gesehen am 27.04.2021
Physical Description:Online Resource
ISSN:1476-5403
DOI:10.1038/sj.cdd.4400692

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