Interleukin-23 promotes a distinct CD4 T cell activation state characterized by the production of interleukin-17
Interleukin-23 promotes a distinct CD4 T cell activation state characterized by the production of interleukin-17
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DOI：
10.1074/jbc.m207577200
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发表时间：
2003-01-17
影响因子：
4.8
通讯作者：
Gurney, AL
中科院分区：
文献类型：
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作者：
Aggarwal, S;Ghilardi, N;Gurney, AL
白细胞介素（IL）-17是一种促炎细胞因子，由活化的T细胞产生。尽管越来越多的证据表明，高水平的IL - 17与包括类风湿性关节炎、银屑病和多发性硬化症在内的几种慢性炎症性疾病有关，但其表达的调控尚未得到很好的表征。我们观察到，对最近描述的细胞因子IL - 23作出反应时，IL - 17的产生会增加。我们提供的证据表明，由活化的树突状细胞产生的鼠源IL - 23作用于记忆T细胞，导致IL - 17分泌增加。IL - 23还诱导相关细胞因子IL - 17F的表达。IL - 23是一种异二聚体细胞因子，与IL - 12共享一个亚基p40。与IL - 23相反，IL - 12对IL - 17的产生只有微小的影响。这些数据表明，在二次免疫应答过程中，IL - 23可以促进一种具有不同于特征明确的Th1和Th2型特征的活化状态。
Interleukin (IL)-17 is a pro-inflammatory cytokine that is produced by activated T cells. Despite increasing evidence that high levels of IL-17 are associated with several chronic inflammatory diseases including rheumatoid arthritis, psoriasis, and multiple sclerosis, the regulation of its expression is not well characterized. We observe that IL-17 production is increased in response to the recently described cytokine IL-23. We present evidence that murine IL-23, which is produced by activated dendritic cells, acts on memory T cells, resulting in elevated IL-17 secretion. IL-23 also induced expression of the related cytokine IL-17F. IL-23 is a heterodimeric cytokine and shares a subunit, p40, with IL-12. In contrast to IL-23, IL-12 had only marginal effects on IL-17 production. These data suggest that during a secondary immune response, IL-23 can promote an activation state with features distinct from the well characterized Th1 and Th2 profiles.