ArticleMediators of inflammation2022
IL-33/ST2 Activation Is involved in Ro60-Regulated Photosensitivity in Cutaneous Lupus Erythematosus.
Article in Mediators of inflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 2 citations in OpenAlex.
- Circulating IL-33 as a sensitive alarmin in systemic lupus erythematosus: a biomarker for disease activity and skin-specific manifestations.Scientific reports · 2026Article
- The IL-33/ST2 Axis Promotes Traumatic Heterotopic Ossification by Driving Macrophage and Mast Cell-Mediated Inflammation via Autophagy Defects.International journal of biological sciences · 2026Article
- Topical miRNA Delivery via Elastic Liposomal Formulation: A Promising Genetic Therapy for Cutaneous Lupus Erythematosus (CLE).International journal of molecular sciences · 2025Article
- Knowledge, attitudes, and practices toward biologics among systemic lupus erythematosus patients: a cross-sectional study.Frontiers in public health · 2025Article
- sST2 Levels Show No Association with Helicobacter pylori Infection in Asymptomatic Patients: Implications for Biomarker Research.Digestive diseases and sciences · 2023Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin- (IL-) 33 contributes to various inflammatory processes. IL-33/ST2 activation participates in systemic lupus erythematous via binding to the receptor of Suppression of Tumorigenicity 2 protein (ST2). However, whether IL-33/ST2 interferes with the nosogenesis of cutaneous lupus erythematosus (CLE) has not been reported so far. Herein, we proposed to disclose the impacts on IL-33/ST2 activation and Ro60 on CLE and their potential implications in the photosensitization of CLE cells. IL-33, ST2, and Ro60 in CLE patients' skin lesions were detected. Murine keratinocytes stimulated with or without IL-33 were irradiated by ultraviolet B (UVB), and the levels of Ro60 and inflammation markers were determined. Keratinocytes were cocultured with J774.2 macrophages and stimulated with IL-33 for analysis of chemostasis. The results identified that IL-33, ST2, and downstream inflammation markers were significantly upregulated in CLE lesions with Ro60 overexpression. Additionally, IL-33 treatment promoted the upregulation of Ro60 induced by UVB treatment in murine keratinocytes. Moreover, IL-33 stimulates keratinocytes to induce macrophage migration via enhancing the generation of the chemokine (C-C motif) ligands 17 and 22. Meanwhile, the silencing of ST2 or nuclear factor-kappa B (NF-
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