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The anti-inflammatory sesquiterpene lactone parthenolide suppresses CD95-mediated activation-induced-cell-death in T-cells

Apoptosis is a morphologically distinct form of cell death involved in many physiological and pathological processes. The death receptor CD95 (APO-1/Fas) and its ligand (L) CD95L are critically involved in activation-induced-cell-death (AICD) of activated T-cells. Here we show that the anti-inflamma...

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Hauptverfasser: Li-Weber, Min (VerfasserIn) , Krammer, Peter H. (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: 29 October 2002
In: Cell death and differentiation
Year: 2002, Jahrgang: 9, Heft: 11, Pages: 1256-1265
ISSN:1476-5403
DOI:10.1038/sj.cdd.4401102
Online-Zugang:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1038/sj.cdd.4401102
Verlag, lizenzpflichtig, Volltext: https://www.nature.com/articles/4401102
Volltext
Verfasserangaben:M. Li-Weber, M. Giaisi, S. Baumann, M.K. Treiber and P.H. Krammer
Beschreibung
Zusammenfassung:Apoptosis is a morphologically distinct form of cell death involved in many physiological and pathological processes. The death receptor CD95 (APO-1/Fas) and its ligand (L) CD95L are critically involved in activation-induced-cell-death (AICD) of activated T-cells. Here we show that the anti-inflammatory sesquiterpene lactone parthenolide derived from the European traditional herb-medicine feverfew and many Mexican India medicinal plants suppresses expression of the CD95L and CD95 at the mRNA levels, thus, preventing T-cells from AICD. We demonstrate that parthenolide blocks NF-κB binding to the two NF-κ binding sites of the CD95L promoter and suppresses promoter activity upon T-cell activation. Aberrant expression of CD95 and, particularly CD95L is dangerous and may lead to severe diseases. Our study indicates that parthenolide supports T-cell survival by down-regulating the CD95 system, at least in part, and, therefore, may have therapeutic potential as a new anti-apoptotic substance against AICD in T-cells.
Beschreibung:Gesehen am 15.04.2021
Beschreibung:Online Resource
ISSN:1476-5403
DOI:10.1038/sj.cdd.4401102

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