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Updated: Jan 24, 2026

Author Spotlight: Evaluating Traditional Chinese Therapy for Ankylosing Spondylitis in Mice
Published on: October 27, 2023
TNF-Related Apoptosis-Inducing Ligand Receptor 1 in Patients With Ankylosing Spondylitis
Duygu Temiz Karadag1, Senem Tekeoglu1, Ayten Yazici1
1From the Departments of Rheumatology.
Objectives:
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) belongs to the tumor necrosis factor (TNF) superfamily and is reported to play a role in autoimmune diseases. In this study, we aimed to measure serum TRAIL receptor 1 (TRAIL-R1) concentration and assess any phenotypic relationship in patients with ankylosing spondylitis (AS).
Methods:
Fifty-three patients with AS were recruited from August 2014 to December 2014 cross-sectionally. Fifty-three sex- and age-matched healthy controls were also recruited. Serum TRAIL-R1 concentrations were measured using an enzyme-linked immunosorbent assay. The association between serum TRAIL-R1, TNF-α, disease activity indices, markers of systemic inflammation, and clinical features were evaluated.
Results:
Serum TRAIL-R1 and TNF-α levels were increased in patients with AS compared with healthy controls (4.5 ± 2.3 vs 3.5 ± 2.3 pg/mL, p = 0.036; 3.8 [1.6-7.7] vs 2.0 [0.21-5.7] pg/mL, p = 0.048, respectively). Serum TRAIL-R1 displayed a medium positive correlation with serum TNF-α concentrations (r = 0.412; p = 0.002). Serum TRAIL-R1 concentration was higher in human leucocyte antigen (HLA)-B27-positive patients compared with non-HLA-B27 patients (5.5 ± 2.2 vs 3.1 ± 1.6 pg/mL, p < 0.001). No relationship was found between serum TRAIL-R1 concentration and disease activity scores.
Conclusions:
This study confirms that serum TRAIL-R1 levels are higher in AS patients than healthy controls. The persistence of significantly elevated serum TRAIL-R1 levels, even in patients with low disease activity or after excluding biologic treatment, and the association with HLA-B27 positivity, warrants further investigation due to the unclear role of TRAIL-R1 in the pathophysiology of AS.
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