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The IL-23/IL-17 axis in inflammation
Yoichiro Iwakura, Harumichi Ishigame
Yoichiro Iwakura, Harumichi Ishigame
Published May 1, 2006
Citation Information: J Clin Invest. 2006;116(5):1218-1222. https://doi.org/10.1172/JCI28508.
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Commentary

The IL-23/IL-17 axis in inflammation

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Abstract

IL-23 induces the differentiation of naive CD4+ T cells into highly pathogenic helper T cells (Th17/ThIL-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.

Authors

Yoichiro Iwakura, Harumichi Ishigame

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