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DC Field | Value | Language |
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dc.rights.license | openAccess | - |
dc.contributor.author | Jiang H. | - |
dc.contributor.author | Milovanovic, Marija | - |
dc.contributor.author | Allan D. | - |
dc.contributor.author | Niedbała W. | - |
dc.contributor.author | Besnard A. | - |
dc.contributor.author | Fukada, Sandra | - |
dc.contributor.author | Alves-Filho, Jose Carlos | - |
dc.contributor.author | Togbe D. | - |
dc.contributor.author | Goodyear C. | - |
dc.contributor.author | LININGTON C. | - |
dc.contributor.author | Xu D. | - |
dc.contributor.author | Lukic, Miodrag | - |
dc.contributor.author | Liew F. | - |
dc.date.accessioned | 2021-04-20T16:05:09Z | - |
dc.date.available | 2021-04-20T16:05:09Z | - |
dc.date.issued | 2012 | - |
dc.identifier.issn | 0014-2980 | - |
dc.identifier.uri | https://scidar.kg.ac.rs/handle/123456789/10566 | - |
dc.description.abstract | Interleukin (IL)-33, a member of the IL-1 cytokine family, is an important modulator of the immune system associated with several immune-mediated disorders. High levels of IL-33 are expressed by the central nervous system (CNS) suggesting a potential role of IL-33 in autoimmune CNS diseases. We have investigated the expression and function of IL-33 in the development of experimental autoimmune encephalomyelitis (EAE) in mice. We report here that IL-33 and its receptor ST2 (IL-33Rα) are highly expressed in spinal cord tissue, and ST2 expression is markedly increased in the spinal cords of mice with EAE. Furthermore, ST2-deficient (ST2-/-) mice developed exacerbated EAE compared with wild-type (WT) mice while WT, but not ST2-/- EAE mice treated with IL-33 developed significantly attenuated disease. IL-33-treated mice had reduced levels of IL-17 and IFN-γ but produced increased amounts of IL-5 and IL-13. Lymph node and splenic macrophages of IL-33-treated mice showed polarization toward an alternatively activated macrophage (M2) phenotype with significantly increased frequency of MR+PD-L2+ cells. Importantly, adoptive transfer of these IL-33-treated macrophages attenuated EAE development. Our data therefore demonstrate that IL-33 plays a therapeutic role in autoimmune CNS disease by switching a predominantly pathogenic Th17/Th1 response to Th2 activity, and by polarization of anti-inflammatory M2 macrophages. © 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim. | - |
dc.rights | info:eu-repo/semantics/openAccess | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/4.0/ | - |
dc.source | European Journal of Immunology | - |
dc.title | IL-33 attenuates EAE by suppressing IL-17 and IFN-γ production and inducing alternatively activated macrophages | - |
dc.type | article | - |
dc.identifier.doi | 10.1002/eji.201141947 | - |
dc.identifier.scopus | 2-s2.0-84864002777 | - |
Appears in Collections: | Faculty of Medical Sciences, Kragujevac |
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10.1002-eji.201141947.pdf | 1.24 MB | Adobe PDF | ![]() View/Open |
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