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-α, 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.

中文翻译：

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强直性脊柱炎患者IL-23 / IL-17途径的生物学和遗传学评估。

强直性脊柱炎是慢性炎性疾病组中最常见的形式，称为脊椎关节炎。CD4 + Th17细胞和IL-23 / IL-17轴的最新发现改变了许多自身免疫性疾病的范例。在这项研究中，我们旨在评估在强直性脊柱炎发病机理中IL-23 / IL-17途径和IL-23受体多态性的重要性。这项研究的血液样本来自109名强直性脊柱炎患者和40名健康对照者。通过ELISA法测定血清TNF-α，IL-6，IL-17和IL-23的水平。IL-23R基因多态性rs11209026（Arg381Gln）和rs4131362（Val362Ile）通过Sanger测序法进行。活动性和非活动性强直性脊柱炎组的IL-6水平均高于对照组。然而，患者组中IL-17和IL-23的水平较低。患者中IL-23R基因rs11209026和rs4131362多态性的频率分别为3.7％和8.3％。结果，强直性脊柱炎患者全身循环中IL-17和IL-23水平降低引起的IL-23 / IL-17信号通路失调，可能通过全身性产生导致疾病的发病慢性自身免疫性炎症。