ArticleFrontiers in endocrinology2019
IL-33 Ameliorates the Development of MSU-Induced Inflammation Through Expanding MDSCs-Like Cells.
Article in Frontiers in endocrinology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Article
- The genetics of gout: translation into clinical practice.Therapeutic advances in musculoskeletal disease · 2025Review
- Review
- Article
- Hybrid cytokine IL233 renders protection in murine acute graft vs host disease (aGVHD).Cellular immunology · 2021Article
- IL-33 in Rheumatic Diseases.Frontiers in medicine · 2021Review
- IL-33 enhances macrophage release of IL-1β and promotes pain and inflammation in gouty arthritis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020Article
- IL-33/ST2 induces neutrophil-dependent reactive oxygen species production and mediates gout pain.Theranostics · 2020Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin-33 (IL-33), a member of the IL-1 superfamily, has been shown to play a critical role in many diseases through regulating the immune cell responses, including myeloid-derived suppressor cells (MDSCs). Our previous study demonstrated that IL-33 might play a protective role in kidney injury in gout patients by regulating the lipid metabolism. However, the role of IL-33in the development of MSU-induced inflammation remains elusive. In this study, an increased IL-33 expression was observed in gout patients, which was positively correlated with inflammatory marker CRP. To explore the effects and mechanisms of the increased IL-33 expression in the gout patients, the anti-ST2 antibody and exogenous recombinant IL-33 were used in MSU-induced peritonitis animal model that mimics human gout. Compared with control group, mice with exogenous recombinant IL-33 significantly ameliorated the inflammatory cells infiltration, while blockage of IL-33 signaling by anti-ST2 had no effect on the development of MSU-induced peritonitis. Furthermore, the crucial inflammatory cytokine IL-1β was markedly decreased in IL-33-treated mice. Besides that, a large number of anti-inflammatory MDSCs with CD11b
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