Targeting IL-33 in autoimmunity and inflammation

J Pharmacol Exp Ther. 2015 Jul;354(1):24-31. doi: 10.1124/jpet.114.222505. Epub 2015 Apr 23.

Abstract

Interleukin-33 (IL-33) belongs to the IL-1 family of cytokines. Whereas IL-1 is processed and released by live immune cells in response to infection or other triggers, IL-33 is mostly released as a danger signal ("alarmin") from damaged cells. IL-33 may also be processed and released from activated mast cells (MCs) with subsequent autocrine and paracrine actions. IL-33 augments the stimulatory effects of IgE and substance P on MCs but can also trigger release of cytokines from MCs on its own. Blood IL-33 levels are increased in asthma, atopic dermatitis, multiple sclerosis, rheumatoid arthritis, and Sjögren's syndrome. However, prolonged elevation of IL-33 downregulates FcεRI and may be protective in atherosclerosis, suggesting different roles in immune-regulated diseases. Even though neutralizing IL-33, knocking-down its receptor, or using its soluble "decoy" receptor has resulted in anti-inflammatory effects, there appear to be different outcomes in different tissues. Hence, selective regulation of IL-33 synthesis, release, and signaling may be required to provide effective treatment options.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Autoimmune Diseases / immunology
  • Autoimmune Diseases / metabolism*
  • Gene Expression Regulation
  • Humans
  • Hypersensitivity / immunology
  • Hypersensitivity / metabolism
  • Inflammation / immunology
  • Inflammation / metabolism*
  • Interleukin-33
  • Interleukins / genetics
  • Interleukins / metabolism*
  • Mast Cells / immunology
  • Mast Cells / metabolism
  • Receptors, Interleukin / metabolism

Substances

  • IL33 protein, human
  • Interleukin-33
  • Interleukins
  • Receptors, Interleukin