ArticleInflammation2023
Interleukin-33/ST2 Axis as Potential Biomarker and Therapeutic Target in Kawasaki Disease.
Article in Inflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- IL-33 blockade attenuates vascular inflammation in a mouse model of Kawasaki disease vasculitis.Clinical and experimental immunology · 2026Article
- The Etiopathogenesis of Kawasaki Disease: Evolving Understanding of Diverse Triggers.Immunity, inflammation and disease · 2025Review
- The Significance of Elevated sST2 in Children with Kawasaki Disease.Children (Basel, Switzerland) · 2025Article
- Impact ofFrontiers in gastroenterology (Lausanne, Switzerland) · 2024Review
- Unraveling the gut: the pivotal role of intestinal mechanisms in Kawasaki disease pathogenesis.Frontiers in immunology · 2024Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Kawasaki disease (KD) is an acute, self-limiting, febrile systemic vasculitis of unknown cause associated with the development of coronary artery lesions (CALs) during childhood. Damage-associated molecular patterns (DAMPs) from cell death and oxidative stress have been shown to be involved in the development of KD vasculitis. Interleukin (IL)-33 is released from damaged endothelial cells and acts as a DAMP. We studied whether IL-33 and its receptor (ST2) might be involved in KD pathogenesis. Serum levels of soluble ST2 (sST2) in KD patients were measured before their first therapy. Furthermore, we investigated the impact of IL-33 on human coronary artery endothelial cells (HCAECs). Serum levels of sST2 were significantly higher in KD patients with CALs than in those with normal coronary arteries. In vitro, IL-33 upregulated the expression of ST2L and increased production of sST2, IL-6, IL-8, and monocyte chemoattractant protein-1 in HCAECs in a time- and concentration-dependent manner. Moreover, IL-33 induced significantly greater production of IL-6 and IL-8 in HCAECs compared to the condition stimulated with isoconcentration of tumor necrosis factor-α. The results of the present study suggest that the IL-33/ST2 axis might be involved in the development of KD vasculitis. The IL-33/ST2 axis may be a therapeutic target for the treatment of KD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.