Role of interleukin-13 in fibrosis, particularly systemic sclerosis

Authors

  • Steven O'Reilly

    Corresponding author
    1. Musculoskeletal Research Group, Institute of Cellular Medicine, Faculty of Medicine, Newcastle University, Newcastle upon Tyne, UK
    • Address for correspondence: Dr. Steven O'Reilly, Ph.D., Musculoskeletal Research Group, Institute of Cellular Medicine, Faculty of Medicine, Newcastle University, Framlington place, NE2 4HH Newcastle upon Tyne, UK. Tel.: 44 191224126; Fax: 44 1912228128; E-mail: steven.o'reilly@newcastle.ac.uk.

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Abstract

Chronic inflammation can lead to altered extracellular matrix deposition and ultimately fibrosis. Interleukin-13 (IL-13) is a cytokine that was found to promote IgE class switching and inhibit proinflammatory cytokines. However, it is now recognized as an important mediator in allergy and most importantly fibrosis. Indeed, animal studies with genetically deleted mice have demonstrated its critical role in fibrosis and although it shares over lapping functions with IL-4 it is the dominant cytokine in fibrosis. Systemic sclerosis is an autoimmune disease in which there is chronic inflammation and fibrosis. The disease is associated with a Th2 polarization and IL-13 levels are elevated both in the blood and in the skin of patients. This review will examine the role of IL-13 in driving fibrosis with a particular emphasis on systemic sclerosis as a prototypical fibrotic disease. It will highlight recent research into the role of IL-13 and how this cytokine may be targeted in systemic sclerosis. © 2013 BioFactors, 39(6):593–596, 2013

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