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International Immunology Advance Access originally published online on December 21, 2007
International Immunology 2008 20(2):209-214; doi:10.1093/intimm/dxm135
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© The Japanese Society for Immunology. 2007. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Differential roles for IFN-{gamma} and IL-17 in experimental autoimmune uveoretinitis

Takeru Yoshimura1,2, Koh-Hei Sonoda1, Yoshiyuki Miyazaki3, Yoichiro Iwakura4, Tatsuro Ishibashi1, Akihiko Yoshimura2 and Hiroki Yoshida3

1 Department of Ophthalmology, Graduate School of Medical Sciences, Kyushu University, Fukuoka
2 Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka
3 Department of Biomolecular Sciences, Faculty of Medicine, Saga University, Saga
4 Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, Tokyo, Japan

Correspondence to: H. Yoshida; E-mail: yoshidah{at}med.saga-u.ac.jp

IL-17-producing CD4+ T cells, so called Th17 cells, constitute a newly identified inflammatogenic cell population, which is critically involved in some inflammatory diseases. To explore the role of Th17 cells in murine experimental autoimmune uveoretinitis (EAU), a model of human autoimmune uveitis where Th1 responses predominantly participate in the pathogenesis, IL-17–/– mice were immunized with interphotoreceptor retinoid-binding protein peptide 1–20 for disease induction. Funduscopic examination revealed that EAU was induced in IL-17–/– mice just like in wild-type (WT) mice at early phases of the disease. However, at later/maintenance phases, the severity was significantly reduced in IL-17–/– mice. Expression of IFN-{gamma} and MCP-1 was comparable between WT and IL-17–/– mice during the time course. In vivo blockade of IFN-{gamma} and IL-4 resulted in exacerbation of EAU at later phases with augmented IL-17 production. Taken together, our data demonstrated that IL-17/Th17 participates in the late phases of EAU and also that Th1 and Th17 responses are differentially required for EAU.

Keywords: autoimmunity, cytokines, inflammation, Th1, Th17

Transmitting editor: T. Watanabe

Received 27 April 2007, accepted 22 November 2007.


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