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Verfasst von:Liang, Jie [VerfasserIn]   i
 Jahraus, Beate [VerfasserIn]   i
 Balta, Emre [VerfasserIn]   i
 Ziegler, Jacqueline D. [VerfasserIn]   i
 Hübner, Katrin [VerfasserIn]   i
 Blank, Norbert [VerfasserIn]   i
 Niesler, Beate [VerfasserIn]   i
 Wabnitz, Guido H. [VerfasserIn]   i
 Samstag, Yvonne [VerfasserIn]   i
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 RORt 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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