Article Text

PDF
IL-33: a Janus cytokine
  1. F Y Liew1,2
  1. 1Institute of Infection, Immunity and Inflammation, University of Glasgow, UK
  2. 2Center of Excellence in Genomic Medicine Research, King Abdulaziz University, Jeddah, Saudi Arabia
  1. Correspondence to Professor Foo Y Liew, Institute of Infection, Immunity and Inflammation, University of Glasgow, 120, University Place, Glasgow G12 8TA, UK; foo.liew{at}glasgow.ac.uk

Abstract

Interleukin (IL) 33, a member of the IL-1 family, is the ligand of ST2 that is expressed mainly on activated Th2 cells and mast cells. IL-33 can skew a predominantly Th1 cell population to a mainly Th2 cells phenotype in vivo. IL-33 messenger RNA is expressed early during infection of the intestinal-dwelling nematode Trichuris muris in mice. IL-33 treatment enhances resistance to Trichuris infection. IL-33 also effectively attenuates sepsis by mobilising the innate cells, neutrophils, to the site of infection, helping to clear the pathogens. Thus, IL-33 may be evolutionally preserved for the host defence against infections. IL-33 can reduce an ongoing atherosclerosis in ApoE−/− mice and attenuate adipocytes mainly by inducing the production of type II cytokines. In contrast, IL-33 can also exacerbate allergy and the inflammation in collagen-induced or serum-induced arthritis. Hence, IL-33 is a double-edged sword, and targeting IL-33 should be approached with caution.

Statistics from Altmetric.com

Footnotes

  • Competing interests None.

  • Provenance and peer review Commissioned; externally peer reviewed.

Request permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.