IL-33 attenuates EAE by suppressing IL-17 and IFN-γ production and inducing alternatively activated macrophages
Jiang, Hui-Rong and Milovanović, Marija and Allan, Debbie and Niedbala, Wanda and Besnard, Anne-Galle and Fukada, Sandra Y and Alves-Filho, Jose C and Togbe, Dieudonnée and Goodyear, Carl S and Linington, Christopher and Xu, Damo and Lukic, Miodrag L and Liew, Foo Y (2012) IL-33 attenuates EAE by suppressing IL-17 and IFN-γ production and inducing alternatively activated macrophages. European Journal of Immunology, 42 (7). 1804–1814. (https://doi.org/10.1002/eji.201141947)
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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.
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Item type: Article ID code: 40390 Dates: DateEventJuly 2012Published12 June 2012Published OnlineNotes: © 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim. Subjects: Medicine > Pharmacy and materia medica Department: Faculty of Science > Strathclyde Institute of Pharmacy and Biomedical Sciences Depositing user: Pure Administrator Date deposited: 10 Jul 2012 12:45 Last modified: 28 Sep 2024 16:32 URI: https://strathprints.strath.ac.uk/id/eprint/40390