Research Papers: Immunology:
Anti-inflammatory effects of interleukin-23 receptor cytokine-binding homology region rebalance T cell distribution in rodent collagen-induced arthritis
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Wei Guo1, Dongmei Yu1, Xin Wang1, Cheng Luo1, Yucong Chen1, Wen Lei1, Chen Wang1, Yaoyao Ge1, Wenyao Xue1, Qiqi Tian1, Xiangdong Gao1 and Wenbing Yao1
1 State Key Laboratory of Natural Medicines, School of Life Science and Technology, China Pharmaceutical University, Nanjing, China
Xiangdong Gao, email:
Wenbing Yao, email:
Keywords: collagen-induced arthritis, IL-23, Th17, Treg, Th9, Immunology and Microbiology Section, Immune response, Immunity
Received: March 09, 2016 Accepted: April 28, 2016 Published: May 11, 2016
IL-23 is an important cytokine to regulate Th17 cell differentiation and promote the proliferation of inflammatory cells in Th17-mediated autoimmune diseases. The collagen-induced arthritis (CIA) in rat is a model of rheumatoid arthritis characterized by pronounced inflammatory auto-responses from B and T cells, especially Th17 cells in lesions. In the present study, we used rhIL23R-CHR to block the IL-23 signaling pathway to probe the importance of IL-23 in misbalancing the ratio of Th17/Th9/Treg cells in CIA rats. After treatments with rhIL23R-CHR, the CIA rats showed a significant decrease of secretions of IL-17 and IL-9, whereas FoxP3 was activated in the process, indicating that IL-23 can manipulate the balance of Th17/Th9/Treg cells. Similar to the animal model, IL-23 also possessed remarkable proinflammatory effects on human fibroblast-like synoviocyte cells (HFLS), showing synergetic outcomes with TNF-α. Together, IL-23 could act as a modulator to imbalance the ratio of Th17/Th9/Treg cells, and rhIL23R-CHR could serve as a potential therapeutic agent for RA patients.
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