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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2009-6-22
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pubmed:abstractText |
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 regulatory 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 RORgammat 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.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/(T,G)-A-L,
http://linkedlifedata.com/resource/pubmed/chemical/IL17A protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-17,
http://linkedlifedata.com/resource/pubmed/chemical/Nuclear Receptor Subfamily 1...,
http://linkedlifedata.com/resource/pubmed/chemical/Peptides,
http://linkedlifedata.com/resource/pubmed/chemical/RORC protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Retinoic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Thyroid Hormone,
http://linkedlifedata.com/resource/pubmed/chemical/Rorc protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/STAT3 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Stat3 protein, mouse
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
1550-6606
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
1
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pubmed:volume |
183
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
246-53
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:19542436-Amino Acid Sequence,
pubmed-meshheading:19542436-Animals,
pubmed-meshheading:19542436-Cell Differentiation,
pubmed-meshheading:19542436-Cells, Cultured,
pubmed-meshheading:19542436-Coculture Techniques,
pubmed-meshheading:19542436-Encephalomyelitis, Autoimmune, Experimental,
pubmed-meshheading:19542436-Humans,
pubmed-meshheading:19542436-Injections, Subcutaneous,
pubmed-meshheading:19542436-Interleukin-17,
pubmed-meshheading:19542436-Male,
pubmed-meshheading:19542436-Mice,
pubmed-meshheading:19542436-Mice, Inbred C57BL,
pubmed-meshheading:19542436-Mice, Knockout,
pubmed-meshheading:19542436-Molecular Sequence Data,
pubmed-meshheading:19542436-Nuclear Receptor Subfamily 1, Group F, Member 3,
pubmed-meshheading:19542436-Peptides,
pubmed-meshheading:19542436-Phosphorylation,
pubmed-meshheading:19542436-Receptors, Retinoic Acid,
pubmed-meshheading:19542436-Receptors, Thyroid Hormone,
pubmed-meshheading:19542436-STAT3 Transcription Factor,
pubmed-meshheading:19542436-T-Lymphocytes, Helper-Inducer
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pubmed:year |
2009
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pubmed:articleTitle |
Regulatory properties of copolymer I in Th17 differentiation by altering STAT3 phosphorylation.
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pubmed:affiliation |
Institute of Health Sciences, Shanghai JiaoTong University School of Medicine, China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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