ArticleMolecular and cellular biochemistry2024
Elevated serum IL-36γ levels in patients with ankylosing spondylitis and its association with disease activity.
Article in Molecular and cellular biochemistry, 2024. 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, 1 citations in OpenAlex.
- The role and predictive value of Th17/Treg imbalance and inflammatory factors in sagittal imbalance after VCD for ankylosing spondylitis.Journal of medical biochemistry · 2025Article
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6 authors at 2 institutions in 1 country.
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Abstract
Ankylosing spondylitis (AS) is a chronic autoimmune disease. The purpose of this study was to investigate the levels of serum IL-36γ in AS patients and their association with AS. The study enrolled 131 subjects, including 45 with active AS, 46 with inactive AS, and 40 healthy controls (HCs). The basic clinical information of each participant was obtained through physical examination and relevant clinical medical records. Serum IL-36γ levels were detected through an enzyme-linked immunosorbent assay. Serum IL-36γ levels in the active AS group were significantly higher than those in the HC group (94.72 vs. 65.76 pg/mL, P = 0.0087). The serum IL-36γ concentration in the inactive AS group was increased as compared to that in the HC group (100.90 vs. 65.76 pg/mL, P = 0.0138). Correlation analysis indicated that serum IL-36γ was positively correlated with glutamyl transferase in the active AS group (P = 0.0172), while serum IL-36γ was positively correlated with uric acid in the inactive AS group (P = 0.0151). The area under the curve (AUC) for IL-36γ was 0.6824 (P = 0.0009), and the AUC for IL-36γ combined with the erythrocyte sedimentation rate and C-reactive protein levels was 0.8102 (P < 0.0001), according to receiver operating characteristic curve analysis. This study found that serum IL-36γ levels were elevated in AS patients and correlated with disease activity. Our results suggest that IL-36γ may be involved in the progression of AS disease and is a potential biomarker for AS.
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