Review ARTICLE

Front. Immunol., 12 March 2012 | doi: 10.3389/fimmu.2012.00020

SOCS, inflammation, and autoimmunity

Akihiko Yoshimura1*, Mayu Suzuki1, Ryota Sakaguchi1, Toshikatsu Hanada1 and Hideo Yasukawa2
  • 1 Department of Microbiology and Immunology, Keio University School of Medicine, Shinanomachi, Tokyo, Japan
  • 2 Division of Cardiovascular Medicine, Kurume University School of Medicine, Kurume, Japan

Cytokines play essential roles in innate and adaptive immunity. However, excess cytokines or dysregulation of cytokine signaling will cause a variety of diseases, including allergies, autoimmune diseases, inflammation, and cancer. Most cytokines utilize the so-called Janus kinase–signal transducers and activators of transcription pathway. This pathway is negatively regulated by various mechanisms including suppressors of cytokine signaling (SOCS) proteins. SOCS proteins bind to JAK or cytokine receptors, thereby suppressing further signaling events. Especially, suppressor of cytokine signaling-1 (SOCS1) and SOCS3 are strong inhibitors of JAKs, because these two contain kinase inhibitory region at the N-terminus. Studies using conditional knockout mice have shown that SOCS proteins are key physiological as well as pathological regulators of immune homeostasis. Recent studies have also demonstrated that SOCS1 and SOCS3 are important regulators of helper T cell differentiation and functions. This review focuses on the roles of SOCS1 and SOCS3 in T cell mediated inflammatory diseases.

Keywords: cytokine, signal transduction, immunity, STAT, helper T cell

Citation: Yoshimura A, Suzuki M, Sakaguchi R, Hanada T and Yasukawa H (2012) SOCS, inflammation, and autoimmunity. Front. Immun. 3:20. doi: 10.3389/fimmu.2012.00020

Received: 31 October 2011; Paper pending published: 16 November 2011;
Accepted: 03 February 2012; Published online: 12 March 2012.

Edited by:

Anna Rubartelli, National Cancer Research Institute, Italy

Reviewed by:

Masaaki Murakami, Osaka University, Japan
Seth Lucian Masters, Walter and Eliza Hall Institute, Australia
Cristina Albanesi, Istituo Dermopatico dell’Immacolata-IRCCS, Italy

Copyright: © 2012 Yoshimura, Suzuki, Sakaguchi, Hanada and Yasukawa. This is an open-access article distributed under the terms of the Creative Commons Attribution Non Commercial License, which permits non-commercial use, distribution, and reproduction in other forums, provided the original authors and source are credited.

*Correspondence: Akihiko Yoshimura, Department of Microbiology and Immunology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo, 160-8582, Japan. e-mail: yoshimura@a6.keio.jp

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