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The IL-23/IL-17 axis in inflammation
Author(s): Iwakura Y, Ishigame H
Source: JOURNAL OF CLINICAL INVESTIGATION    Volume: 116    Issue: 5    Pages: 1218-1222    Published: MAY 2006  
Times Cited: 178     References: 29     
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-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.
Document Type: Editorial Material
Language: English
Reprint Address: Iwakura, Y (reprint author), Univ Tokyo, Inst Med Sci, Ctr Med Expt, Minato Ku, 4-6-1 Shirokanedai, Tokyo 1088639, Japan
Addresses:
1. Univ Tokyo, Inst Med Sci, Ctr Med Expt, Minato Ku, Tokyo 1088639, Japan
Publisher: AMER SOC CLINICAL INVESTIGATION INC, 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
Subject Category: Medicine, Research & Experimental
IDS Number: 038WH
ISSN: 0021-9738
DOI: 10.1172/JCI28508
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