eISSN: 1644-4124
ISSN: 1426-3912
Central European Journal of Immunology
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4/2019
vol. 44
 
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abstract:
Clinical immunology

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

Hulya Deveci
1
,
Ayla Caglıyan Turk
2
,
Zeliha Cansel Ozmen
3
,
Ayse Kevser Demir
4
,
Safiye Umut Say Coskun
5

  1. Department of Physical Medicine and Rehabilitation, Tokat Gaziosmanpaşa University School of Medicine, Turkey
  2. Department of Physical Medicine and Rehabilitation, Hitit University School of Medicine, Turkey
  3. Department of Biochemistry, Tokat Gaziosmanpaşa University School of Medicine, Turkey
  4. Department of Internal Medicine, Tokat Gaziosmanpaşa University School of Medicine, Turkey
  5. Department of Microbiology, Tokat Gaziosmanpaşa University School of Medicine, Turkey
(Centr Eur Immunol 2019; 44 (4): 433-439)
Online publish date: 2020/01/20
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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-, 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.
keywords:

polymorphism, ankylosing spondylitis, cytokine, IL-17, IL-23, signalling pathways

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