STAT3 and NF-κB Signal Pathway Is Required for IL-23-Mediated IL-17 Production in Spontaneous Arthritis Animal Model IL-1 Receptor Antagonist-Deficient Mice-Reference-Cited by-同舟云学术

STAT3 and NF-κB Signal Pathway Is Required for IL-23-Mediated IL-17 Production in Spontaneous Arthritis Animal Model IL-1 Receptor Antagonist-Deficient Mice

Published:2006-04-18 Issue:9 Volume:176 Page:5652-5661
ISSN:0022-1767
Container-title:The Journal of Immunology
language:en
Short-container-title:J Immunol

Author:

Cho Mi-La,Kang Jung-Won,Moon Young-Mee,Nam Hyo-Jung,Jhun Joo-Yeon,Heo Seong-Beom,Jin Hyun-Tak,Min So-Youn,Ju Ji-Hyeon,Park Kyung-Su,Cho Young-Gyu,Yoon Chong-Hyeon,Park Sung-Hwan,Sung Young-Chul,Kim Ho-Youn

Publisher

The American Association of Immunologists

Subject

Immunology,Immunology and Allergy

Reference50 articles.

1. Interleukin-23 rather than interleukin-12 is the critical cytokine for autoimmune inflammation of the brain

2. Divergent Pro- and Antiinflammatory Roles for IL-23 and IL-12 in Joint Autoimmune Inflammation

3. Role of the IL-12/IL-23 System in the Regulation of T-Cell Responses in Central Nervous System Inflammatory Demyelination;

4. IL-23 drives a pathogenic T cell population that induces autoimmune inflammation

5. New IL-12-family members: IL-23 and IL-27, cytokines with divergent functions

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