IL-27 blocks RORc expression to inhibit lineage commitment of Th17 cells.

作者: Caroline Diveu , Mandy J. McGeachy , Katia Boniface , Jason S. Stumhofer , Manjiri Sathe

DOI: 10.4049/JIMMUNOL.0801162

关键词:

摘要: IL-27 is secreted by APCs in response to inflammatory stimuli and exerts a proinflammatory Th1-enhancing activity but also has significant anti-inflammatory functions. We examined the molecular mechanism which regulates TGFbeta plus IL-6- or IL-23-dependent Th17 development mouse human systems. inhibited production of IL-17A IL-17F naive T cells suppressing, STAT1-dependent manner, expression Th17-specific transcription factor RORgamma t. The vivo significance role was addressed delayed-type hypersensitivity experimental autoimmune encephalomyelitis (EAE). By generating mice deficient for p28 subunit IL-27, we showed that regulated severity EAE through its effects on cells. Furthermore, up-regulation IL-10 CNS, usually occurs late after onset plays resolution disease, notably absent IL-27p28(-/-) mice. These results show acts as negative regulator developing vivo, suggesting potential therapeutic diseases.

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