Biological and genetic evaluation of IL-23/IL-17 pathway in ankylosing spondylitis patients

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dc.contributor.authorDeveci, Hulya
dc.contributor.authorTurk, Ayla Cagliyan
dc.contributor.authorOzmen, Zeliha Cansel
dc.contributor.authorDemir, Ayse Kevser
dc.contributor.authorCoskun, Safiye Umut Say
dc.date.accessioned2021-11-01T15:02:00Z
dc.date.available2021-11-01T15:02:00Z
dc.date.issued2019
dc.department[Belirlenecek]
dc.description.abstractAnkylosing 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.
dc.identifier.doi10.5114/ceji.2019.92805
dc.identifier.endpage439en_US
dc.identifier.issn1426-3912
dc.identifier.issn1644-4124
dc.identifier.issue4en_US
dc.identifier.pmid32140056
dc.identifier.scopus2-s2.0-85082200711
dc.identifier.scopusqualityQ3
dc.identifier.startpage433en_US
dc.identifier.urihttps://doi.org/10.5114/ceji.2019.92805
dc.identifier.urihttps://hdl.handle.net/11491/6803
dc.identifier.volume44en_US
dc.identifier.wosWOS:000517818400012
dc.identifier.wosqualityN/A
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.institutionauthor[Belirlenecek]
dc.language.isoen
dc.publisherTermedia Publishing House Ltd
dc.relation.ispartofCentral European Journal Of Immunology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectpolymorphismen_US
dc.subjectankylosing spondylitisen_US
dc.subjectcytokineen_US
dc.subjectIL-17en_US
dc.subjectIL-23en_US
dc.subjectsignalling pathwaysen_US
dc.titleBiological and genetic evaluation of IL-23/IL-17 pathway in ankylosing spondylitis patients
dc.typeArticle

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