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Role of IL-33/ST2 signaling pathway in systemic sclerosis and other fibrotic diseases

1, 2, 3, 4

  1. Department of Rheumatology and Immunology, Peking University People’s Hospital, Beijing, China.
  2. Strathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, Glasgow, UK.
  3. Strathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, Glasgow, UK.
  4. Department of Rheumatology and Immunology, Peking University People’s Hospital, Beijing, China. murongster@163.com

CER12008 Submission on line
2019 Vol.37, N°4 ,Suppl.119 - PI 0141, PF 0146
Reviews

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Rheumatology Article

 

Abstract

Systemic sclerosis (SSc) is a complex autoimmune disease characterised by fibrosis of the skin and multiple internal organs. Interleukin 33 (IL-33) has recently been investigated as a potential key player in the pathogenesis of SSc and other fibrotic diseases, owing to its effects on tissue fibrosis. Understanding how IL-33 is regulated and how it contributes to the development of fibrosis will be important to elucidate disease pathogenesis and may shed light on new areas for therapeutic development for patients. Here we discuss the recent research progress in our understanding of the role and the underlying mechanisms of IL-33/ST2 signaling pathway in SSc and other fibrotic diseases.

PMID: 31498062 [PubMed]

Received: 20/12/2018 - Accepted : 03/06/2019 - In Press: 03/09/2019 - Published: 03/10/2019