The IL-23/IL-17 axis in inflammation

被引：822

作者：

Iwakura, Y ^{[1
]}

Ishigame, H ^{[1
]}

机构：

[1] Univ Tokyo, Inst Med Sci, Ctr Med Expt, Minato Ku, Tokyo 1088639, Japan

来源：

JOURNAL OF CLINICAL INVESTIGATION | 2006年 / 116卷 / 05期

关键词：

D O I：

10.1172/JCI28508

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

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-alpha, but not IFN-gamma 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-gamma 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.

引用

页码：1218 / 1222

页数：5

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