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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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Bibliographische Detailangaben
Hauptverfasser: Wendling, Uwe (VerfasserIn) , Walczak, Henning (VerfasserIn) , Krammer, Peter H. (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: 27 June 2000
In: Cell death and differentiation
Year: 2000, Jahrgang: 7, Heft: 7, Pages: 637-644
ISSN:1476-5403
DOI:10.1038/sj.cdd.4400692
Online-Zugang:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1038/sj.cdd.4400692
Verlag, lizenzpflichtig, Volltext: https://www.nature.com/articles/4400692
Volltext
Verfasserangaben:U. Wendling, H. Walczak, J. Dörr, C. Jaboci, M. Weller, P.H. Krammer and F. Zipp
Beschreibung
Zusammenfassung: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.
Beschreibung:Gesehen am 27.04.2021
Beschreibung:Online Resource
ISSN:1476-5403
DOI:10.1038/sj.cdd.4400692

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