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    Biological and genetic evaluation of IL-23/IL-17 pathway in ankylosing spondylitis patients
    (Termedia Publishing House Ltd, 2019) Deveci, Hulya; Turk, Ayla Cagliyan; Ozmen, Zeliha Cansel; Demir, Ayse Kevser; Coskun, Safiye Umut Say
    Ankylosing spondylitis is the most common form of the chronic inflammatory disease group known as spondyloarthritides. Recent discoveries of the CD4+ Th17 cells and IL-23/IL-17 axis have changed the paradigms in many autoimmune diseases. In this study, we aimed to evaluate the importance of IL-23/IL-17 pathway and IL-23 receptor polymorphism in the pathogenesis of ankylosing spondylitis. Blood samples for this study were obtained from 109 ankylosing spondylitis patients and 40 healthy control subjects. Serum levels of TNF-alpha, IL-6, IL-17, and IL-23 were measured by the ELISA method. The IL-23R gene polymorphisms rs11209026 (Arg381Gln) and rs4131362 (Val362Ile) were performed by the Sanger Sequence method. IL-6 levels were higher in the active and inactive ankylosing spondylitis groups than in the control group. However, levels of IL-17 and IL-23 were lower in the patient group. The frequency of IL-23R gene rs11209026 and rs4131362 polymorphism were 3.7% and 8.3% in the patient, respectively. As a result, dysregulation of the IL-23 / IL-17 pathway, which is caused by reduced levels of IL-17 and IL-23 in systemic circulation in patients with ankylosing spondylitis, may contribute to the pathogenesis of the disease by systemically producing chronic autoimmune inflammation.
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    Serum Interleukin-23/17 Levels in Ankylosing Spondylitis Patients Treated with Nonsteroidal Anti-Inflammatory Drugs: A Prospective Cohort Study
    (Mary Ann Liebert, Inc, 2019) Deveci, Hulya; Turk, Ayla Cagliyan; Ozmen, Zeliha Cansel; Deveci, Koksal
    Etiopathogenesis of ankylosing spondylitis (AS), a major subtype of a group of chronic inflammatory diseases known as spondyloarthropathies, is not clearly understood yet. In this study, we aimed to investigate the interleukin 23 (IL-23)/interleukin-17 (IL-17) pathway, which is a new cytokine pathway in inflammatory diseases. We evaluated serum IL-17 and IL-23 levels after 1-year follow-up in AS patients using only nonsteroidal anti inflammatory drugs (at need or continue). Forty-four AS patients and 40 healthy controls were included in the study. Clinical evaluations of disease activity were performed. Serum tumor necrosis factor-alpha (TNF-alpha), IL-6, IL-17, and IL-23 levels were evaluated. IL-17 and IL-23 levels of the patient group at baseline and 12 months were lower than the control group. There was no significant difference between the baseline and 12th month evaluations of the patient group. TNF-alpha levels were similar in all groups (in the baseline and 12th month of the patient group and in the control group). Although our results are in contrast to the literature findings, the IL-23/IL-17 pathway is a newly discovered pathway, and there may still be unknowns. New studies involving larger patient groups are needed for the factors affecting serum IL-23/IL-17 levels in patients with AS. We also think that it will be useful to make more comprehensive and long-term studies about which patients will respond well to IL-23/IL-17 blockade.