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IL-33 blockade suppresses the development of experimental autoimmune encephalomyelitis in C57BL/6 mice
- Source :
-
Journal of Neuroimmunology . Jun2012, Vol. 247 Issue 1/2, p25-31. 7p. - Publication Year :
- 2012
-
Abstract
- Abstract: IL-33 is a recently described member of the IL-1 family that has been reported to have a pathogenic role in several inflammatory diseases. In this study, we evaluated the role of IL-33 in a murine model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE). We showed that the expression of IL-33 and its receptor, ST2, was markedly elevated in the spinal cord of mice during myelin oligodendrocyte glycoprotein (MOG)35–55 peptide-induced EAE. Administration of a blocking anti-IL-33 antibody in mice of EAE during the induction phase significantly inhibited the onset and severity of EAE and reduced MOG35–55-induced IFN-γ and IL-17 production. In contrast, treatment with recombinant IL-33 worsened the disease course of EAE in association with increased induction of both IFN-γ and IL-17. Furthermore, anti-IL-33 treatment caused a remarkable decrease in expression of IL-17, IFN-γ, T-bet and RORγt, and an upregulation of IL-10 and TGF-β in the spinal cord of EAE mice. These results demonstrate that endogenous IL-33 plays a pivotal role in the pathogenesis of EAE and indicate that blockade of IL-33 has a significant protective effect against EAE. [Copyright &y& Elsevier]
Details
- Language :
- English
- ISSN :
- 01655728
- Volume :
- 247
- Issue :
- 1/2
- Database :
- Academic Search Index
- Journal :
- Journal of Neuroimmunology
- Publication Type :
- Academic Journal
- Accession number :
- 75168267
- Full Text :
- https://doi.org/10.1016/j.jneuroim.2012.03.016