Anti-inflammatory effects of interleukin-23 receptor cytokine-binding homology region rebalance T cell distribution in rodent collagen-induced arthritis.
Anti-inflammatory effects of interleukin-23 receptor cytokine-binding homology region rebalance T cell distribution in rodent collagen-induced arthritis.
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IL-23 受体细胞因子结合同源区的抗炎作用在啮齿动物胶原诱导的关节炎中重新平衡 T 细胞分布。
DOI:
10.18632/oncotarget.9309
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发表时间:
2016-05-31
期刊:
影响因子:
--
通讯作者:
Yao W
中科院分区:
文献类型:
--
作者:
Guo W;Yu D;Wang X;Luo C;Chen Y;Lei W;Wang C;Ge Y;Xue W;Tian Q;Gao X;Yao W
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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影响因子:
64.5
作者:
Ivanov, Ivaylo I.;McKenzie, Brent S.;Littman, Dan R.
通讯作者:
Littman, Dan R.
DOI:
10.1038/nri2580
发表时间:
2009-07
期刊:
Nature reviews. Immunology
影响因子:
--
作者:
通讯作者:
--
影响因子:
--
作者:
Guo W;Wang C;Wang X;Luo C;Yu D;Wang Y;Chen Y;Lei W;Gao X;Yao W
通讯作者:
Yao W
影响因子:
5.4
作者:
Chen, Li;Wei, Xiao-Qing;Aeschlimann, Daniel
通讯作者:
Aeschlimann, Daniel
影响因子:
5.7
作者:
Andersson, Karin M. E.;Cavallini, Nicola Filluelo;Bokarewa, Maria I.
通讯作者:
Bokarewa, Maria I.