Strathprints logo
Strathprints Home | Open Access | Browse | Search | User area | Copyright | Help | Library Home | SUPrimo

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.

Full text not available in this repository. (Request a copy from the Strathclyde author)

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.

Item type: Article
ID code: 40390
Notes: © 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
Keywords: experimental autoimmune encephalomyelitis , IL-33, M2 macrophages, Th17/Th1, Pharmacy and materia medica, Immunology, Immunology and Allergy
Subjects: Medicine > Pharmacy and materia medica
Department: Faculty of Science > Strathclyde Institute of Pharmacy and Biomedical Sciences
Related URLs:
    Depositing user: Pure Administrator
    Date Deposited: 10 Jul 2012 13:45
    Last modified: 09 May 2014 05:12
    URI: http://strathprints.strath.ac.uk/id/eprint/40390

    Actions (login required)

    View Item