Deveci, HulyaTurk, Ayla CagliyanOzmen, Zeliha CanselDemir, Ayse KevserCoskun, Safiye Umut Say2021-11-012021-11-0120191426-39121644-4124https://doi.org/10.5114/ceji.2019.92805https://hdl.handle.net/11491/6803Ankylosing 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.eninfo:eu-repo/semantics/openAccesspolymorphismankylosing spondylitiscytokineIL-17IL-23signalling pathwaysArticle44443343910.5114/ceji.2019.92805N/AWOS:0005178184000122-s2.0-8508220071132140056Q3