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Usage Information

The IL-23/IL-17 axis in inflammation
Yoichiro Iwakura, Harumichi Ishigame
Yoichiro Iwakura, Harumichi Ishigame
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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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Usage data is cumulative from November 2025 through November 2026.

Usage JCI PMC
Text version 2,496 1,160
PDF 401 141
Figure 760 0
Citation downloads 324 0
Totals 3,981 1,301
Total Views 5,282
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Usage information is collected from two different sources: this site (JCI) and Pubmed Central (PMC). JCI information (compiled daily) shows human readership based on methods we employ to screen out robotic usage. PMC information (aggregated monthly) is also similarly screened of robotic usage.

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ISSN: 0021-9738 (print), 1558-8238 (online)

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