No abstract

These findings indicated a role of IL-28B in RA and it may contribute to avoiding osteoclasia in RA patients.

Objectives:This study aims to determine the changes in serum levels of type-III interferons (type-III IFNs) in ankylosing spondylitis (AS) patients treated with tumor necrosis factor-alpha inhibitors (TNFi) and analyze the correlations between serum type-III IFN levels and disease activity. Patients and methods:The study included 57 AS patients (51 males, 6 females; mean age 29.7±7.0 years; range, 18 to 50 years), who had been diagnosed with AS and had active disease before the start of the study (median disease duration: four years, range 1.3 to 8.0 years). Control group included 50 healthy, age-and sex-matched individuals (45 males, 5 females; mean age 25.5±6.7 years; range, 18 to 55 years). The enzyme-linked immunosorbent assay was used to assess the serum interleukin (IL)-29, IL-28A, and IL-28B levels of AS patients at baseline and first, third, sixth months after treatment with TNFi. Clinical and laboratory features of the disease were also evaluated for AS patients at baseline and first, third, sixth months after treatment. Results: Serum IL-28A levels were significantly higher in AS patients (354.8±164.0 pg/mL) than in controls (257.2±99.6, p=0.003) at baseline. Serum IL-28B levels were significantly lower in AS patients (median, 491.4 pg/mL, range 296.6 to 944.6 pg/mL) than in controls (1121.1±409.3 pg/mL, p=0.000) at baseline. Serum IL-29 levels at third month after treatment (median 430.9, range 277.4 to 1023.9 pg/mL) were significantly increased compared with baseline (median 399.1, range 261.2 to 826.7 pg/mL), p=0.002) and controls (335.2±100.5 pg/mL, p=0.041). There was no association between serum type-III IFN levels and disease activity indexes at baseline. Serum levels of IL-28A were negatively correlated with erythrocyte sedimentation rate levels at first and sixth months after treatment (r=-0.266, p=0.046; r=-0.286, p=0.034, respectively). Serum levels of IL-28A were negatively correlated with Bath Ankylosing Spondylitis Disease Activity Index at third month after treatment (r=-0.269, p=0.043). Serum levels of IL-29 were negatively correlated with Bath Ankylosing Spondylitis Disease Activity Index at third month after treatment (r=-0.299, p=0.024). There was a significant increasing trend for serum IL-28B after TNFi treatment in AS patients, opposite to the decreasing trend for disease activity. Conclusion: These findings indicate that type-III IFNs may be involved in the pathogenesis of AS. Thus, type-III IFNs may provide new targets for the treatment of AS.