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

被引:251
|
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
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
收藏
页码:670 / 675
页数:6
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