Changes and significance of IL-25 in chicken collagen II-induced experimental arthritis (CIA)

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• 作者：Wang Kaiwen (1)
  Su Zhaoliang (1)
  Zhao Yinxia (1)
  Sandoghchian Shotorbani Siamak (1)
  Jiao Zhijun (2)
  Xue Yuan (1)
  Yang Heng (1)
  Zheng Dong (1)
  Liu Yanfang (1)
  Shen Pei (1)
  Wang Shengjun (1)
  Shao Qixiang (1)
  Huang Xinxiang (1)
  Lu Liwei (3)
  Xu Huaxi (1)
  
• 关键词：Collagen II ; induced experimental arthritis (CIA) ; IL ; 25 ; IL ; 17 ; IL ; 4 ; DBA/1 mice
• 刊名：Rheumatology International
• 出版年：2012
• 出版时间：August 2012
• 年：2012
• 卷：32
• 期：8
• 页码：2331-2338
• 全文大小：715KB
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• 作者单位：Wang Kaiwen (1)
  Su Zhaoliang (1)
  Zhao Yinxia (1)
  Sandoghchian Shotorbani Siamak (1)
  Jiao Zhijun (2)
  Xue Yuan (1)
  Yang Heng (1)
  Zheng Dong (1)
  Liu Yanfang (1)
  Shen Pei (1)
  Wang Shengjun (1)
  Shao Qixiang (1)
  Huang Xinxiang (1)
  Lu Liwei (3)
  Xu Huaxi (1)
  
  1. Department of Immunology, Institute of Laboratory Medicine, Jiangsu University, 212013, Zhenjiang, People鈥檚 Republic China
  2. Department of Laboratory Medicine, The Central Laboratory, Affiliated Hospital of Jiangsu University, Zhenjiang, People鈥檚 Republic China
  3. Department of Pathology, Hong Kong University, Hongkong, People鈥檚 Republic China
  

文摘

Rheumatoid arthritis (RA) is an autoimmune inflammatory disease. It is a systemic inflammatory disease, characterized by chronic, symmetrical, multi-articular synovial arthritis. IL-25 (IL-17E) is a member of the recently emerged cytokine family (IL-17s), which is expressed in Th2 cells and bone marrow-derived mast cells. Unlike the other members of this family, IL-25 is capable of inducing Th2-associated cytokines (IL-4, IL-5, and IL-13) and also promotes the release of some pro-immune factors (IL-6 and IL-8). IL-25 is also a pleiotropic factor, which constitutes a tissue-specific pathological injury and chronic inflammation. In this study, we used chicken collagen II-induced experimental arthritis (CIA) model in DBA/1 mice to investigate the relationship between IL-25 and other inflammatory factors, revealing the possible mechanism in CIA. Our results showed that the expression level of IL-25 was enhanced in the late stage of CIA, and IL-17 was increased in the early stage of the disease. It is well known that IL-17 has a crucial role in the development of RA pathogenesis, and IL-25 plays a significant role in humoral immune. For reasons given above, we suggested that the IL-25 inhibited IL-17 expression to some extent, while enhancing the production of IL-4. It was confirmed that IL-25 not only regulated the cellular immune, but also involved the humoral immune in rheumatoid arthritis.