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Curr Opin Immunol. 2006 Dec;18(6):670-5. Epub 2006 Sep 28.

The IL-23/Th(17) axis: therapeutic targets for autoimmune inflammation.

Author information

1
Eli Lilly and Company, Indianapolis, IN 46285, USA.

Erratum in

  • Curr Opin Immunol. 2007 Feb;19(1):111.

Abstract

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-beta1 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.

PMID:
17010592
DOI:
10.1016/j.coi.2006.09.008
[Indexed for MEDLINE]

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