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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| Main Authors: | , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
29 October 2002
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| In: |
Cell death and differentiation
Year: 2002, Volume: 9, Issue: 11, Pages: 1256-1265 |
| ISSN: | 1476-5403 |
| DOI: | 10.1038/sj.cdd.4401102 |
| Online Access: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1038/sj.cdd.4401102 Verlag, lizenzpflichtig, Volltext: https://www.nature.com/articles/4401102 
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| Author Notes: | M. Li-Weber, M. Giaisi, S. Baumann, M.K. Treiber and P.H. Krammer |
| Summary: | 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. |
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| Item Description: | Gesehen am 15.04.2021 |
| Physical Description: | Online Resource |
| ISSN: | 1476-5403 |
| DOI: | 10.1038/sj.cdd.4401102 |