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Scand J Immunol. 2008 Dec;68(6):589-97. doi: 10.1111/j.1365-3083.2008.02174.x.

IL-17 eliminates the therapeutic effects of myelin basic protein-induced nasal tolerance in experimental autoimmune encephalomyelitis by activating IL-6.

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1
Department of Neurobiology, Harbin Medical University Provincial Key Lad of Neurobiology, Harbin, Heilongjiang, China.

Abstract

Interleukin (IL)-17 is a proinflammatory cytokine primarily secreted by Th17 cells, which are a CD4(+) T-cell subset. Th17 cells and IL-17 are important in the pathogenesis of multiple sclerosis and in its established animal model, experimental autoimmune encephalomyelitis (EAE). However, it is unclear whether IL-17 contributes to EAE immune tolerance. We used the myelin basic protein (MBP) peptide MBP 68-86 to induce nasal tolerance to EAE, and simultaneously interfered with the tolerance by treatment with different doses of IL-17. We found that IL-17 dramatically interfered with MBP 68-86-induced immune tolerance. IL-17 administration increased IL-6 release, skewing T cell differentiation towards Th17 cells and decreasing the number of Treg cells. This led to an imbalance between Treg cells and Th17 cells and spurred the development of EAE.

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