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Interleukin-33 in Systemic Sclerosis: Expression and Pathogenesis.

Liya Li1,2, Honglin Zhu1,2, Xiaoxia Zuo1,2

  • 1Department of Rheumatology and immunology, Xiangya Hospital, Central South University, Changsha, China.

Frontiers in Immunology
|December 1, 2018
PubMed
Summary
This summary is machine-generated.

Interleukin-33 (IL-33) acts as an alarmin cytokine. This review explores IL-33's role in systemic sclerosis pathogenesis and its potential as a clinical target for this fibrotic disease.

Keywords:
ST2fibrosisinterleukin-33pathogenesissystemic sclerosis

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Area of Science:

  • Immunology
  • Rheumatology
  • Cell Biology

Background:

  • Interleukin-33 (IL-33) is an IL-1 superfamily member with cytokine and nuclear functions.
  • IL-33 acts as an alarmin, mediating effects via ST2 receptor and IL-1 receptor accessory protein.
  • Emerging evidence suggests IL-33 is a pro-fibrotic cytokine and a potential target for systemic sclerosis.

Purpose of the Study:

  • To review the current understanding of IL-33's role in systemic sclerosis.
  • To focus on the pleiotropic expression and pathogenesis of IL-33 in this disease.
  • To evaluate the feasibility of IL-33 as a clinical application for systemic sclerosis.

Main Methods:

  • Literature review of existing research on IL-33 and systemic sclerosis.
  • Analysis of IL-33's expression patterns and biological functions.
  • Assessment of IL-33's involvement in the pathogenesis of systemic sclerosis.

Main Results:

  • IL-33 plays a significant role in the immune system and fibrotic processes.
  • IL-33 interacts with ST2 and IL-1 receptor accessory protein, affecting immune cells.
  • IL-33 is implicated in the development and progression of systemic sclerosis.

Conclusions:

  • IL-33 is an emerging pro-fibrotic cytokine with a key role in systemic sclerosis.
  • Targeting IL-33 may offer a novel therapeutic strategy for systemic sclerosis.
  • Further research is needed to explore the clinical feasibility of IL-33 inhibition.