SOCS, inflammation, and autoimmunity

Akihiko Yoshimura, Mayu Suzuki, Ryota Sakaguchi, Toshikatsu Hanada, Hideo Yasukawa

Research output: Contribution to journalReview article

149 Citations (Scopus)

Abstract

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 Nterminus. 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.

Original languageEnglish
Article numberArticle 20
JournalFrontiers in Immunology
Volume3
Issue numberMAR
DOIs
Publication statusPublished - 2012 Dec 1

Keywords

  • Cytokine
  • Helper T cell
  • Immunity
  • STAT
  • Signal transduction

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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