Медицинская иммунология (Jun 2018)

INTERLEUKIN 33 AND FIBROSIS: PATHOGENESIS UPDATED

  • E. G. Uchasova,
  • O. V. Gruzdeva,
  • Yu. A. Dileva,
  • V. N. Karetnikova

DOI
https://doi.org/10.15789/1563-0625-2018-4-477-484
Journal volume & issue
Vol. 20, no. 4
pp. 477 – 484

Abstract

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Interleukin 33 (IL-33) is a member of the IL-1 family, which is widely expressed on all types of cells. IL-33 was identified as a functional ligand for the plasma membrane receptor complex, which is a heterodimer consisting of a membrane bound ST2 receptor (growth stimulating factor). IL-33 is involved in the development of immune response with predominant release of pro-inflammatory T helper type 2 cytokines. IL-33 is widely expressed on various structure-forming cells, such as epithelial, endothelial and smooth muscle cells. Increased expression of IL-33 is observed during necrosis of these cells (after tissue or cell damage), and it is released into extracellular space, and acts as an endogenous danger signal, sending a sort of warnings to neighboring cells and tissues. Recently, many studies have shown that IL-33 can participate in development and progression of fibrosis in various organs. However, it exerts anti-inflammatory effects upon development of other diseases. This review will discuss biological characteristics of IL-33 and a role of the IL-33/ST2 signaling pathway in the development of fibrosis.

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