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Interleukin-17 Promotes Autoimmunity by Triggering a Positive-Feedback Loop via Interleukin-6 Induction. (Associate Prof. Murakami and Prof. Hirano in Immunity)

Dysregulated cytokine expression and signaling are major contributors to a number of autoimmune diseases. Interleukin-17A (IL-17A) and IL-6 are important in many disorders characterized by immune self-recognition,and IL-6 is known to induce the differentiation of T helper 17 (Th17) cells.

The authors described an IL-17A-triggered positive-feedback loop of IL-6 signaling, which involved the activation of the transcription factors nuclear factor (NF)-kB and signal transducer and activator of transcription 3 (STAT3) in fibroblasts. Importantly, enhancement of this loop caused by disruption of suppressor of cytokine signaling 3 (SOCS3)-dependent negative regulation of the IL-6 signal transducer gp130 contributed to the development of arthritis.

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Because this mechanism also enhanced experimental autoimmune encephalomyelitis (EAE) in wild-type mice, it may be a general etiologic process underlying other Th17 cell-mediated autoimmune diseases.


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Contact:

Toshio Hirano
Laboratory of Developmental Immunology,
Graduate School of Frontier Biosciences, Graduate School of Medicine
and WPI Immunology Frontier Research Center, Osaka University, JST, CREST
2-2 Yamada-oka, Suita, Osaka 565-0871, Japan

Tel: +81-6-6879-3881 Fax:+81-6-6875-3889
E-mail: hirano@molonc.med.osaka-u.ac.jp

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