ArticleFrontiers in medicine2025
Expression of Tim-3 on neutrophils as a novel indicator to assess disease activity and severity in ankylosing spondylitis.
Article in Frontiers in medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Neutrophil extracellular traps and acute kidney injury: a narrative review.Frontiers in immunology · 2026Review
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12 authors.
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Abstract
Objective: To investigate the expression of Tim-3 on neutrophils in ankylosing spondylitis (AS) patients and its correlation with disease activity, severity, and inflammatory markers. Methods: Sixty-two AS patients from Guangdong Second Provincial General Hospital and 38 healthy controls (HC) were enrolled. Clinical data, physical exams, and laboratory measurements were recorded. Flow cytometry measured Tim-3 and PD-1 expression on neutrophils, real-time PCR quantified mRNA levels and protein expression of Tim-3 was determined by Western blot. We analyzed the correlation between Tim-3 mean fluorescence intensity (MFI) on neutrophils, inflammatory markers, and AS disease activity and severity. Results: Tim-3 expression on neutrophils was higher in AS patients than in HC, showing a positive correlation with erythrocyte sedimentation rate (ESR), c-reactive protein (CRP), and Ankylosing Spondylitis Disease Activity Score (ASDAS). Active AS patients (ASDAS ≥ 1.3) had increased Tim-3 MFI compared to inactive ones (ASDAS < 1.3). Regular treatment with non-steroidal anti-inflammatory drugs (NSAIDs), biological disease-modifying anti-rheumatic drugs (bDMARDs), and conventional synthetic disease-modifying anti-rheumatic drugs (csDMARDs) over a month significantly reduced Tim-3 MFI in AS patients. Conclusion: Elevated Tim-3 expression on neutrophils correlates with increased inflammatory markers and AS activity. Treatment lowered Tim-3 MFI, suggesting its potential as an indicator for assessing AS disease activity and severity and as a feedback mechanism to reduce tissue damage from inflammation.
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