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IL‐17 Eliminates the Therapeutic Effects of Myelin Basic Protein‐Induced Nasal Tolerance in Experimental Autoimmune Encephalomyelitis by Activating IL‐6
Author(s) -
Wang G.Y.,
Sun B.,
Kong Q.F.,
Zhang Y.,
Li R.,
Wang J.H.,
Wang D.D.,
Lv G. X.,
Li H.L.
Publication year - 2008
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.2008.02174.x
Subject(s) - experimental autoimmune encephalomyelitis , myelin basic protein , immunology , encephalomyelitis , medicine , myelin , multiple sclerosis , endocrinology , central nervous system
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.