J Clin Invest 116(5): 1218-1222

The IL-23/IL-17 axis in inflammation

Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, Tokyo, Japan.

Address correspondence to: Yoichiro Iwakura, Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan. Phone: 81-3-5449-5536; Fax: 81-3-5449-5430; E-mail: pj.ca.oykot-u.smi@arukawi .

Abstract

IL-23 induces the differentiation of naive CD4^{T cells into highly pathogenic helper T cells (Th17/Th}_IL-17) that produce IL-17, IL-17F, IL-6, and TNF-α, but not IFN-γ and IL-4. Two studies in this issue of the JCI demonstrate that blocking IL-23 or its downstream factors IL-17 and IL-6, but not the IL-12/IFN-γ pathways, can significantly suppress disease development in animal models of inflammatory bowel disease and MS (see the related articles beginning on pages 1310 and 1317). These studies suggest that the IL-23/IL-17 pathway may be a novel therapeutic target for the treatment of chronic inflammatory diseases.

Abstract

Acknowledgments

We would like to thank Shigeru Kakuta and Susumu Nakae (Stanford University School of Medicine, Stanford, California, USA) for critical reading of the manuscript.

Acknowledgments

Footnotes

Nonstandard abbreviations used: CIA, collagen-induced arthritis; IBD, inflammatory bowel disease; IL-1Ra, IL-1 receptor antagonist; R, receptor.

Conflict of interest: The authors have declared that no conflict of interest exists.

Citation for this article:J. Clin. Invest.116:1218–1222 (2006). doi:10.1172/JCI28508.

See the related article beginning on page 1310.

Footnotes

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