The IL-23/Th17axis:: therapeutic targets for autoimmune inflammation

被引：254

作者：

Kikly, Kristine ^{[1
]}

Liu, Ling ^{[1
]}

Na, Songqing ^{[1
]}

Sedgwick, Jonathon D. ^{[1
]}

机构：

[1] Eli Lilly & Co, Indianapolis, IN 46285 USA

来源：

CURRENT OPINION IN IMMUNOLOGY | 2006年 / 18卷 / 06期

关键词：

D O I：

10.1016/j.coi.2006.09.008

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Autoimmune inflammatory responses and the diseases that develop as a consequence are now thought to be driven through a novel non-Th-1 pathway. IL-23, together with additional factors including TGF-beta 1 and IL-6, collectively generate and sustain a distinct CD4(+) 'Th-17 inflammation effector' T-cell subset characterized by its production of inflammatory chemokines and cytokines, including IL-17. With this paradigm shift in understanding of autoimmune inflammation pathogenesis comes exciting opportunities to identify and to target therapeutically molecules within the IL-23/Th-17 axis that are key to disease development.

引用

页码：670 / 675

页数：6

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