IL-6 in Inflammation, Immunity, and Disease

  1. Tadamitsu Kishimoto4
  1. 1Department of Clinical Application of Biologics, Osaka University Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan
  2. 2Department of Immunopathology, World Premier International Immunology Frontier Research Center, Osaka University, Osaka 565-0871, Japan
  3. 3Department of Respiratory Medicine, Allergy and Rheumatic Diseases, Osaka University Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan
  4. 4Laboratory of Immune Regulation, World Premier International Immunology Frontier Research Center, Osaka University, Osaka 565-0871, Japan
  1. Correspondence: kishimoto{at}ifrec.osaka-u.ac.jp

Abstract

Interleukin 6 (IL-6), promptly and transiently produced in response to infections and tissue injuries, contributes to host defense through the stimulation of acute phase responses, hematopoiesis, and immune reactions. Although its expression is strictly controlled by transcriptional and posttranscriptional mechanisms, dysregulated continual synthesis of IL-6 plays a pathological effect on chronic inflammation and autoimmunity. For this reason, tocilizumab, a humanized anti-IL-6 receptor antibody was developed. Various clinical trials have since shown the exceptional efficacy of tocilizumab, which resulted in its approval for the treatment of rheumatoid arthritis and juvenile idiopathic arthritis. Moreover, tocilizumab is expected to be effective for other intractable immune-mediated diseases. In this context, the mechanism for the continual synthesis of IL-6 needs to be elucidated to facilitate the development of more specific therapeutic approaches and analysis of the pathogenesis of specific diseases.



Also in this Collection

      | Table of Contents

      This Article

      1. Cold Spring Harb. Perspect. Biol. 6: a016295 Copyright © 2014 Cold Spring Harbor Laboratory Press; all rights reserved

      Article Category

      Updates/Comments

      1. Submit Updates/Comments
      2. No Updates/Comments published

      Subject Collections

      1. Innate Immunity and Inflammation

      Share

      In this Collection