Mitochondrial reactive oxygen species control T cell activation by regulating IL-2 and IL-4 expression: mechanism of ciprofloxacin-mediated immunosuppression
This article shows that T cell activation-induced expression of the cytokines IL-2 and -4 is determined by an oxidative signal originating from mitochondrial respiratory complex I. We also report that ciprofloxacin, a fluoroquinolone antibiotic, exerts immunosuppressive effects on human T cells supp...
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| Hauptverfasser: | , , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
May 01 2010
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| In: |
The journal of immunology
Year: 2010, Jahrgang: 184, Heft: 9, Pages: 4827-4841 |
| ISSN: | 1550-6606 |
| DOI: | 10.4049/jimmunol.0901662 |
| Online-Zugang: | Resolving-System, lizenzpflichtig, Volltext: https://doi.org/10.4049/jimmunol.0901662 Verlag, lizenzpflichtig, Volltext: https://journals.aai.org/jimmunol/article/184/9/4827/83235/Mitochondrial-Reactive-Oxygen-Species-Control-T 
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| Verfasserangaben: | Marcin M. Kamiński, Sven W. Sauer, Claus-Detlev Klemke, Dorothee Süss, Jürgen G. Okun, Peter H. Krammer, Karsten Gülow |
MARC
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| 520 | |a This article shows that T cell activation-induced expression of the cytokines IL-2 and -4 is determined by an oxidative signal originating from mitochondrial respiratory complex I. We also report that ciprofloxacin, a fluoroquinolone antibiotic, exerts immunosuppressive effects on human T cells suppressing this novel mechanism. Sustained treatment of preactivated primary human T cells with ciprofloxacin results in a dose-dependent inhibition of TCR-induced generation of reactive oxygen species (ROS) and IL-2 and -4 expression. This is accompanied by the loss of mitochondrial DNA and a resulting decrease in activity of the complex I. Consequently, using a complex I inhibitor or small interfering RNA-mediated downregulation of the complex I chaperone NDUFAF1, we demonstrate that TCR-triggered ROS generation by complex I is indispensable for activation-induced IL-2 and -4 expression and secretion in resting and preactivated human T cells. This oxidative signal (H2O2) synergizes with Ca2+ influx for IL-2/IL-4 expression and facilitates induction of the transcription factors NF-κB and AP-1. Moreover, using T cells isolated from patients with atopic dermatitis, we show that inhibition of complex I-mediated ROS generation blocks disease-associated spontaneous hyperexpression and TCR-induced expression of IL-4. Prolonged ciprofloxacin treatment of T cells from patients with atopic dermatitis also blocks activation-induced expression and secretion of IL-4. Thus, our work shows that the activation phenotype of T cells is controlled by a mitochondrial complex I-originated oxidative signal. | ||
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