Regulatory Properties of Copolymer I in Th17 Differentiation by Altering STAT3 Phosphorylation
Regulatory Properties of Copolymer I in Th17 Differentiation by Altering STAT3 Phosphorylation
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DOI：
10.4049/jimmunol.0900193
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发表时间：
2009-07-01
影响因子：
4.4
通讯作者：
Zhang, Jingwu Z.
中科院分区：
文献类型：
--
作者：
Chen, Chunhua;Liu, Xuebin;Zhang, Jingwu Z.
Th17 and Th1 play an important role in multiple sclerosis for which copolymer I (COP-I) is a treatment option. We described here that the treatment effect of COP-I correlated with its unique regulator, properties on differentiation and survival of Th17 in experimental autoimmune encephalomyelitis mice, which was mediated through down-regulation of STAT3 phosphorylation. The effect of COP-I on Th17 differentiation required CD14(+) monocytes through IL-6 signaling as a key mediator to regulate STAT3 phosphorylation and subsequent ROR gamma t expression in Th17 cells. The observed effect was markedly dampened when monocytes were genetically deficient for IL-6. Similar regulatory properties of COP-I were demonstrated in human Th17 differentiation. The study revealed the differential regulatory roles and the novel mechanism of action of COP-I chiefly responsible for its treatment efficacy in experimental autoimmune encephalomyelitis and multiple sclerosis. The Journal of Immunology, 2009, 183: 246-253.
