The Journal of Experimental Medicine
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Published online
doi:10.1084/jem.20071119
The Journal of Experimental Medicine, Vol. 205, No. 10, 2281-2294
The Rockefeller University Press, 0022-1007 $30.00
© Sonderegger et al.
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ARTICLE

 GM-CSF mediates autoimmunity by enhancing IL-6–dependent Th17 cell development and survival

Ivo Sonderegger1, Giandomenica Iezzi1, Reinhard Maier2, Nicole Schmitz3, Michael Kurrer4, and Manfred Kopf1

1 Institute of Integrative Biology, Molecular Biomedicine, ETH Zürich, 8952 Zürich, Switzerland
2 Research Department, Kantonal Hospital, 9007 St. Gallen, Switzerland
3 Cytos Biotechnology AG, 8952 Schlieren, Switzerland
4 Department of Pathology, University Zürich, 8091 Zürich, Switzerland

CORRESPONDENCE Manfred Kopf: Manfred.Kopf{at}ethz.ch

Granulocyte macrophage–colony stimulating factor (GM-CSF) is critically involved in development of organ-related autoimmune inflammatory diseases including experimental allergic encephalitis and collagen-induced arthritis. Roles of GM-CSF in the initiation and in the effector phase of the autoimmune response have been proposed. Our study was designed to investigate the mechanisms of GM-CSF in autoimmunity using a model of autoimmune heart inflammatory disease (myocarditis). The pathological sequel after immunization with heart myosin has been shown previously to depend on IL-1, IL-6, IL-23, and IL-17. We found that innate GM-CSF was critical for IL-6 and IL-23 responses by dendritic cells and generation of pathological Th17 cells in vivo. Moreover, GM-CSF promoted autoimmunity by enhancing IL-6–dependent survival of antigen specific CD4+ T cells. These results suggest a novel role for GM-CSF in promoting generation and maintenance of Th17 cells by regulation of IL-6 and IL-23 in vivo.

Abbreviations used: EAE, experimental allergic encephalitis; EAM, experimental autoimmune myocarditis; GM-CSF, granulocyte macrophage–colony stimulating factor; myhc{alpha}, myosin heavy chain {alpha}; PAMP, Pathogen associated molecular pattern; PI, propidium iodide; TLR, toll-like receptor.

© 2008 Sonderegger et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jem.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).


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