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The Journal of Immunology, 2009, 182, 3183 -3190
Copyright © 2009 by The American Association of Immunologists, Inc.
doi:10.4049/jimmunol.0802487

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Anti-Inflammatory Role of IL-17 in Experimental Autoimmune Uveitis1

Yan Ke*, Ke Liu{ddagger}, Guo-Qiang Huang{ddagger}, Yan Cui{dagger}, Henry J. Kaplan*, Hui Shao2,3,* and Deming Sun2,3,{dagger}

* Department of Ophthalmology and Visual Sciences, Kentucky Lions Eye Center, University of Louisville, KY 40202; {dagger} Doheny Eye Institute, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033; and {ddagger} Southern BioTech, Birmingham AL 35209

Previous studies have shown that IL-17 is a strong proinflammatory cytokine and that IL-17-producing autoreactive T cells play a major role in the pathogenesis of autoimmune diseases. In a previous study, we showed that injection of experimental autoimmune uveitis-susceptible mice with anti-IL-17 Abs blocked subsequent disease development. To determine whether administration of IL-17 to experimental autoimmune uveitis-susceptible Lewis rats and B10RIII mice injected with disease-inducing peptides enhanced disease susceptibility, we injected the recipient animals with various doses of human rIL-17 (hIL-17). Unexpectedly, the treated animals showed significant amelioration of disease; in addition, both the intensity of the autoreactive response and cytokine production by the autoreactive T cells induced by immunization with uveitogenic peptides were significantly decreased. Our results show that IL-17 has anti-inflammatory activity and that this cytokine can suppress the development of autoimmune disease.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

1 This work was supported in part by National Institutes of Health Grants EY12974, EY14599, EY014366, and EY017373. D.S. is a recipient of a senior investigator award from Research to Prevent Blindness. H.S. is a recipient of a career development award from Research to Prevent Blindness.

2 H.S. and D.S. contributed equally to this work.

3 Address correspondence and reprint requests to Dr. Deming Sun, Doheny Eye Institute, Keck School of Medicine, University of Southern California, Los Angeles, CA90033 or Dr. Hui Shao, Department of Ophthalmology, University of Louisville, Louisville, KY 40202. E-mail addresses: dsun{at}doheny.org or h0shao01{at}louisville.edu

4 Abbreviations used in this paper: IRBP, interphotoreceptor retinoid-binding protein; EAU, experimental autoimmune uveitis; hIL-17, human IL-17; p.i., postimmunization; PMN, polymorphonuclear neutrophil.







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