| Online-Ressource |
Verfasst von: | Liang, Jie [VerfasserIn]  |
| Jahraus, Beate [VerfasserIn]  |
| Balta, Emre [VerfasserIn]  |
| Ziegler, Jacqueline D. [VerfasserIn]  |
| Hübner, Katrin [VerfasserIn]  |
| Blank, Norbert [VerfasserIn]  |
| Niesler, Beate [VerfasserIn]  |
| Wabnitz, Guido H. [VerfasserIn]  |
| Samstag, Yvonne [VerfasserIn]  |
Titel: | Sulforaphane inhibits inflammatory responses of primary human T-cells by increasing ROS and depleting glutathione |
Verf.angabe: | Jie Liang, Beate Jahraus, Emre Balta, Jacqueline D. Ziegler, Katrin Hübner, Norbert Blank, Beate Niesler, Guido H. Wabnitz and Yvonne Samstag |
E-Jahr: | 2018 |
Jahr: | 14 November 2018 |
Umfang: | 17 S. |
Fussnoten: | Gesehen am 06.12.2018 |
Titel Quelle: | Enthalten in: Frontiers in immunology |
Ort Quelle: | Lausanne : Frontiers Media, 2010 |
Jahr Quelle: | 2018 |
Band/Heft Quelle: | 9(2018), Artikel-ID 2584 |
ISSN Quelle: | 1664-3224 |
Abstract: | The activity and function of T-cells are influenced by the intra- and extracellular redox milieu. Oxidative stress induces hypo-responsiveness of untransformed T-cells. Vice versa increased glutathione (GSH) levels or decreased levels of reactive oxygen species (ROS) prime T-cell metabolism for inflammation, e.g. in rheumatoid arthritis (RA). Therefore, balancing the T-cell redox milieu may represent a promising new option for therapeutic immune modulation. Here we show that sulforaphane (SFN), a compound derived from plants of the Brassicaceae family, e.g. broccoli, induces a pro-oxidative state in untransformed human T-cells of healthy donors or RA patients. This manifested as an increase of intracellular ROS and a marked decrease of GSH. Consistently, increased global cysteine sulfenylation was detected. Importantly, a major target for SFN-mediated protein oxidation was STAT3, a transcription factor involved in the regulation of TH17-related genes. Accordingly, SFN significantly inhibited the activation of untransformed human T-cells derived from healthy donors or RA patients, and specifically downregulated the the transcription factor RORt expression of the TH17-related cytokines IL-17A, IL-17F, and IL-22, which play a major role within the pathophysiology of many chronic inflammatory/autoimmune diseases. The inhibitory effects of SFN could be abolished by exogenous supplied GSH and the GSH replenishing antioxidant N-acetyl-cysteine (NAC). Together, our study provides mechanistic insights into the mode of action of the natural substance sulforaphane. It specifically exerts TH17 prone immunosuppressive effects on untransformed human T-cells by decreasing GSH and accumulation of ROS. Thus, SFN may offer novel clinical options for the treatment of TH17 related chronic inflammatory/autoimmune diseases such as rheumatoid arthritis. |
DOI: | doi:10.3389/fimmu.2018.02584 |
URL: | kostenfrei: Volltext ; Verlag: http://dx.doi.org/10.3389/fimmu.2018.02584 |
| kostenfrei: Volltext: https://www.frontiersin.org/articles/10.3389/fimmu.2018.02584/full |
| DOI: https://doi.org/10.3389/fimmu.2018.02584 |
Datenträger: | Online-Ressource |
Sprache: | eng |
Sach-SW: | Glutathione |
| Primary human T-cells |
| Reactive Oxygen Species |
| Rheumatoid arthritis |
| Sulforaphane |
| Th17 |
K10plus-PPN: | 1584917741 |
Verknüpfungen: | → Zeitschrift |
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Lokale URL UB: | Zum Volltext |
Sulforaphane inhibits inflammatory responses of primary human T-cells by increasing ROS and depleting glutathione / Liang, Jie [VerfasserIn]; 14 November 2018 (Online-Ressource)