ArticleArthritis research & therapy2020
Elevated serum levels of checkpoint molecules in patients with adult Still's disease.
Article in Arthritis research & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 23 citations in OpenAlex.
- Elevated plasma sTIM-3 levels in patients with severe COVID-19.The Journal of allergy and clinical immunology · 2021Trial
- Association of serum TIM-3 and Galectin-9 levels with glaucoma progression: implications for clinical monitoring.American journal of translational research · 2026Article
- Antiretroviral Treatment-Induced Galectin-9 Might Impact HIV Viremia in Addition to Contributing to Inflammaging.International journal of molecular sciences · 2023Article
- Diagnosis and treatment of adult-onset Still's disease: a concise summary of the German society of rheumatology S2 guideline.Zeitschrift fur Rheumatologie · 2023Review
- The Expanding Spectrum of Autoinflammatory Diseases.Internal medicine (Tokyo, Japan) · 2023Article
- Serum soluble T cell immunoglobulin mucin domain-3 as an early predictive marker for severity of acute pancreatitis; a retrospective analysis.BMC gastroenterology · 2022Article
- Increase in Serum Soluble Tim-3 Level Is Related to the Progression of Diseases After Hepatitis Virus Infection.Frontiers in medicine · 2022Article
- Adult-Onset Still's Disease: Novel Biomarkers of Specific Subsets, Disease Activity, and Relapsing Forms.International journal of molecular sciences · 2021Review
- Serum checkpoint molecules in patients with IgG4-related disease (IgG4-RD).Arthritis research & therapy · 2021Article
- Interleukin-18 Is a Potential Biomarker to Discriminate Active Adult-Onset Still's Disease From COVID-19.Frontiers in immunology · 2021Article
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12 authors at 2 institutions in 1 country.
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Abstract
backgroundThe interaction between galectin-9 (Gal-9) and its ligand, T cell immunoglobulin, and mucin-containing-molecule-3 (TIM-3), one of the coinhibitory receptors, transduce the inhibitory signaling to regulate immune responses. The dysregulated expression of checkpoint molecules has been reported under various inflammatory or autoimmune conditions. The aim of this study is to investigate the levels of these checkpoint molecules and their associations between proinflammatory markers in patients with adult Still's disease (ASD).
methodsSerum samples were collected from 47 patients with active ASD, 116 patients with rheumatoid arthritis (RA), and 37 healthy controls (HCs). Serum levels of Gal-9, soluble TIM-3 (sTIM-3), and IL-18 were determined using enzyme-linked immunosorbent assay (ELISA). Results were compared with the clinical features of ASD.
resultsSerum Gal-9 levels in patients with ASD (median: 21.57 ng/ml, interquartile range IQR [11.41-39.72]) were significantly higher compared to those in patients with RA (7.58 ng/ml, IQR [5.57-10.20] p < 0.001) as well as those in HCs (4.51 ng/ml, [IQR; 3.58-5.45], p < 0.001). Similarly, serum sTIM-3 levels in patients with ASD were significantly higher than those in patients with RA and HCs. Serum levels of Gal-9 or sTIM-3 showed positive correlations with IL-18 levels (Gal-9; r = 0.90, p < 0.001, sTIM-3; r = 0.78, p < 0.001) in patients with ASD. Serum levels of Gal-9 or sTIM-3 correlated with serum ferritin (Gal-9; r = 0.77, p < 0.001, sTIM-3; r = 0.71, p < 0.001) and ASD disease activity score (Pouchot's score, Gal-9; r = 0.66, p < 0.001, sTIM-3; r = 0.59, p < 0.001), whereas there was no significant correlation between serum Gal-9 or sTIM-3 and CRP. ASD patients with chronic arthritis phenotype had a significantly higher Gal-9/ferritin and sTIM-3/ferritin ratio than those without this phenotype. After immunosuppressive treatment, Gal-9 and sTIM-3 levels showed a significant decline in parallel to the disease activity scores.
conclusionsSerum levels of the coinhibitory checkpoint molecules were elevated and correlated with disease activity in patients with ASD. These coinhibitory checkpoint molecules may be implicated in the autoinflammatory process seen in ASD.
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