Interleukin 2 Ameliorates Autoimmune Neuroinflammation by Modulating the Balance of T Helper 17 Cells and Regulatory T Cells in Mouse

Objective. Multiple sclerosis (MS) is a progressive autoimmune-mediated inflammation of the central nervous system (CNS), and experimental autoimmune encephalomyelitis (EAE) is a suitable model to study the pathogenesis of MS. IL-2 has been considered as both a T cell growth factor and an anti-inflammatory cytokine. In the present study, we investigated the effects of a low dose IL-2 treatment on mouse EAE therapy. Method The expression of IL-2 and IL-2 receptor were predicted using public micro-array data and verified by real-time PCR and ELISA in mouse EAE model. Mice were injected with Myelin Oligodendrocyte Glycoprotein (35-55)(MOG(35)(-)(55)) subcutaneously to induce EAE model. IL-2 treatment was initiated during 5 consecutive days from day 15 post MOG(35)(-)(55) immunization. Flow cytometry was applied to investigate the proportions of Th17 and Treg cells. ELISA was used to detect the concentrations of IL-17a, IFNr, IL-10 and TGFb. Results. In this study, we showed that the IL-2 treatment ameliorates the clinical severity of EAE. Flow cytometry results indicated that the therapeutic effect was related to a reduction of Th17 cells and an expansion of Treg cells in the EAE spinal cord. In vitro experiments also confirmed the anti-inflammatory effect of IL-2 in EAE-reactivated T cells. Conclusion. Low-dose IL-2 is a potential therapeutic strategy for EAE and MS.

Automated summary

Low-dose IL-2 treatment was shown to ameliorate clinical severity of EAE by reducing Th17 cells and expanding Treg cells in the spinal cord. In vitro experiments confirmed the anti-inflammatory effect of IL-2 in EAE-reactivated T cells. This suggests low-dose IL-2 as a potential therapeutic strategy for EAE and MS.