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Erschienen in: Clinical Rheumatology 2/2011

01.02.2011 | Brief Report

Increased serum IL-17 and IL-23 in the patient with ankylosing spondylitis

verfasst von: Yang Mei, Faming Pan, Jing Gao, Rui Ge, Zhenhua Duan, Zhen Zeng, Fangfang Liao, Guo Xia, Sheng Wang, Shengqian Xu, Jianhua Xu, Li Zhang, Dongqing Ye

Erschienen in: Clinical Rheumatology | Ausgabe 2/2011

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Abstract

Interleukin 17 (IL-17) is a Th17 cytokine associated with inflammation, autoimmunity, and defense against some bacteria; it has been implicated in many chronic autoimmune diseases including psoriasis, multiple sclerosis, and systemic sclerosis. However, whether IL-17 plays a role in the pathogenesis of ankylosing spondylitis (AS) remains unclear. To analyze the content of IL-17 and IL-23 in the serum from patients with AS compared with health control subject, 50 patients with AS and 43 healthy volunteers were recruited. Serum IL-17 levels were examined by enzyme linked immunosorbent assay (ELISA). Statistic analyses were performed by SPSS 13.0. Results show that the serum IL-17 and IL-23 levels were significantly elevated in AS patients as compared with normal controls. Nevertheless, no associations of serum IL-17 and IL-23 levels with clinical and laboratory parameters were found; no significant difference regarding serum IL-17 and IL-23 levels was found between less active AS and more active AS. However, there was a strong positive association between the serum levels of IL-17 and IL-23 in the AS patients. Our results indicate increased serum IL-17 and IL-23 levels in AS patients, suggesting that this two cytokine may play critical roles in the pathogenesis of AS. Therefore, further studies are required to confirm this preliminary data.
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Metadaten
Titel
Increased serum IL-17 and IL-23 in the patient with ankylosing spondylitis
verfasst von
Yang Mei
Faming Pan
Jing Gao
Rui Ge
Zhenhua Duan
Zhen Zeng
Fangfang Liao
Guo Xia
Sheng Wang
Shengqian Xu
Jianhua Xu
Li Zhang
Dongqing Ye
Publikationsdatum
01.02.2011
Verlag
Springer-Verlag
Erschienen in
Clinical Rheumatology / Ausgabe 2/2011
Print ISSN: 0770-3198
Elektronische ISSN: 1434-9949
DOI
https://doi.org/10.1007/s10067-010-1647-4

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