Systemic sclerosis is a complex and poorly understood connective tissue disease characterized
by diffuse fibrosis in several organs, especially the skin (
Asano, 2017
;
Bhattacharyya et al., 2012
;
Denton et al., 2006
). IL-33 is found to regulate tissue fibrosis in multiple organs (
Kotsiou et al., 2018
;
Xu et al., 2016
). However, the exact role of IL-33 in fibrosis remains controversial (
Kotsiou et al., 2018
). Previous studies have shown a profibrotic role for the IL-33 cytokine through its
receptor, IL-1 receptor-like 1 (or ST2), which regulates the secretion of the profibrotic
cytokine, IL-13, from eosinophils, M2 macrophages, and type 2 innate lymphoid cells
(
Li et al., 2014
;
Rankin et al., 2010
;
Wu et al., 2018
). However, IL-33 can also play an antifibrotic role through the induction of type
2 innate lymphoid cells and regulatory T cells in several organs, including the skin
(
Cheon et al., 2022
;
Garbern et al., 2019
;
Riedel et al., 2017
). Thus, it is critical to determine the full spectrum of the IL-33 effect in fibrosis
to develop optimal therapies for its use in the treatment of systemic sclerosis and
other fibrosis-associated diseases.Abbreviations:
BLM (bleomycin), IL-33KO (IL-33 knockout), WT (wild-type)To read this article in full you will need to make a payment
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Article info
Publication history
Published online: January 25, 2023
Accepted manuscript published online XXX; corrected proof published online XXXPublication stage
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© 2023 The Authors. Published by Elsevier, Inc. on behalf of the Society for Investigative Dermatology.