pubmed-article:16906223 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:16906223 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
pubmed-article:16906223 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
pubmed-article:16906223 | lifeskim:mentions | umls-concept:C1332714 | lld:lifeskim |
pubmed-article:16906223 | lifeskim:mentions | umls-concept:C1416467 | lld:lifeskim |
pubmed-article:16906223 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
pubmed-article:16906223 | lifeskim:mentions | umls-concept:C0439836 | lld:lifeskim |
pubmed-article:16906223 | pubmed:issue | 9 | lld:pubmed |
pubmed-article:16906223 | pubmed:dateCreated | 2006-9-6 | lld:pubmed |
pubmed-article:16906223 | pubmed:abstractText | IFN-gamma is an important Th1 proinflammatory cytokine and has a paradoxical effect on EAE in which disease susceptibility is unexpectedly heightened in IFN-gamma-deficient mice. In this study, we provide what we believe is new evidence indicating that IFN-gamma is critically required for the conversion of CD4+ CD25- T cells to CD4+ Tregs during EAE. In our study, the added severity of EAE in IFN-gamma knockout mice was directly associated with altered encephalitogenic T cell responses, which correlated with reduced frequency and function of CD4+ CD25+ Foxp3+ Tregs when compared with those of WT mice. It was demonstrated in both human and mouse systems that in vitro IFN-gamma treatment of CD4+ CD25- T cells led to conversion of CD4+ Tregs as characterized by increased expression of Foxp3 and enhanced regulatory function. Mouse CD4+ CD25- T cells, when treated in vitro with IFN-gamma, acquired marked regulatory properties as evidenced by suppression of EAE by adoptive transfer. These findings have important implications for the understanding of the complex role of IFN-gamma in both induction and self regulation of inflammatory processes. | lld:pubmed |
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pubmed-article:16906223 | pubmed:language | eng | lld:pubmed |
pubmed-article:16906223 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16906223 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:16906223 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16906223 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16906223 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16906223 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16906223 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16906223 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16906223 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16906223 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16906223 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16906223 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:16906223 | pubmed:month | Sep | lld:pubmed |
pubmed-article:16906223 | pubmed:issn | 0021-9738 | lld:pubmed |
pubmed-article:16906223 | pubmed:author | pubmed-author:SunWeiW | lld:pubmed |
pubmed-article:16906223 | pubmed:author | pubmed-author:ChenXiX | lld:pubmed |
pubmed-article:16906223 | pubmed:author | pubmed-author:HongJianJ | lld:pubmed |
pubmed-article:16906223 | pubmed:author | pubmed-author:ZhangJingwu... | lld:pubmed |
pubmed-article:16906223 | pubmed:author | pubmed-author:SunBingB | lld:pubmed |
pubmed-article:16906223 | pubmed:author | pubmed-author:XuLingyunL | lld:pubmed |
pubmed-article:16906223 | pubmed:author | pubmed-author:WangZhaojunZ | lld:pubmed |
pubmed-article:16906223 | pubmed:author | pubmed-author:LiuAilianA | lld:pubmed |
pubmed-article:16906223 | pubmed:author | pubmed-author:LiNingliN | lld:pubmed |
pubmed-article:16906223 | pubmed:author | pubmed-author:XuGuangwuG | lld:pubmed |
pubmed-article:16906223 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:16906223 | pubmed:volume | 116 | lld:pubmed |
pubmed-article:16906223 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:16906223 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:16906223 | pubmed:pagination | 2434-41 | lld:pubmed |
pubmed-article:16906223 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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pubmed-article:16906223 | pubmed:meshHeading | pubmed-meshheading:16906223... | lld:pubmed |
pubmed-article:16906223 | pubmed:year | 2006 | lld:pubmed |
pubmed-article:16906223 | pubmed:articleTitle | Role of IFN-gamma in induction of Foxp3 and conversion of CD4+ CD25- T cells to CD4+ Tregs. | lld:pubmed |
pubmed-article:16906223 | pubmed:affiliation | Joint Immunology Laboratory of Institute of Health Sciences, Shanghai JiaoTong University School of Medicine, and Shanghai Institutes of Biological Sciences, Chinese Academy of Sciences, Shanghai, People's Republic of China. | lld:pubmed |
pubmed-article:16906223 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:16906223 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |