IL-35 Is Involved in the Pathogenesis of Guillain–Barré Syndrome Through Its Influence on the Function of CD4+ T Cells

Abstract

CD4+ T cells and many cytokines play critical roles in the pathogenesis of Guillain–Barré Syndrome (GBS), an immune-mediated inflammatory disease. However, the role of IL-35, a novel member of the IL-12 cytokine family, in this kind of disease has not yet been elucidated. In this study, we investigated the functional changes of CD4+ T cells from GBS patients with IL-35 treatment in vitro. This study involved 21 GBS patients and an equal number of healthy controls (HCs). The results indicated that the average concentration of IL-35 in the plasma of GBS patients was lower than that of healthy controls (HCs). Increased levels of STAT1, STAT3 and STAT4 proteins and T-bet, ROR γt, IFN-γ and IL-17A mRNA were observed in CD4+ T cells from GBS patients. In contrast, the levels of STAT5 and STAT6 proteins and GATA3, Foxp3, IL-4 and TGF-β1 mRNAs were decreased in GBS patients in comparison with those of HCs. In addition, treatment of CD4+ T cells from GBS patients with IL-35 upregulated IL-35, STAT5 and STAT6 protein and T-bet, GATA3, Foxp3, IFN-γ, IL-4, IL-17A and TGF-β1 mRNA while inhibited levels of STAT3 and STAT4 protein and RORγt and IL-17A mRNA. These results indicate that IL-35 might play a potential role in GBS pathogenesis. Further studies are required in order to evaluate its role in GBS.

• CD4+ T cells
• Guillain–Barré Syndrome
• IL-35
• STAT
• transcription factors

Acknowledgements

We thank Zhi-Guo Wu and Jing-Hui Liang for technical assistance.

Declaration of Interest

The authors declare no conflict of interest. The authors alone are responsible for the content and writing of this paper.

This study was supported by Hunan Provincial Project for the Department of Science and Technology for studying Guillain–Barré Syndrome, [2011]102; No. 2011FJ4271.