pubmed-article:19362139 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:19362139 | lifeskim:mentions | umls-concept:C0039198 | lld:lifeskim |
pubmed-article:19362139 | lifeskim:mentions | umls-concept:C0063356 | lld:lifeskim |
pubmed-article:19362139 | lifeskim:mentions | umls-concept:C1817959 | lld:lifeskim |
pubmed-article:19362139 | lifeskim:mentions | umls-concept:C0443199 | lld:lifeskim |
pubmed-article:19362139 | lifeskim:mentions | umls-concept:C1709059 | lld:lifeskim |
pubmed-article:19362139 | lifeskim:mentions | umls-concept:C1515655 | lld:lifeskim |
pubmed-article:19362139 | pubmed:issue | 6 | lld:pubmed |
pubmed-article:19362139 | pubmed:dateCreated | 2009-7-14 | lld:pubmed |
pubmed-article:19362139 | pubmed:abstractText | Inflammation within the Central Nervous System (CNS) is largely controlled by the balance between CNS-specific effector and regulatory T lymphocytes. To suppress CNS-inflammation in an antigen-specific manner, CNS-specific effector and regulatory T cells thus have to be differentially regulated. We employed recombinant peptide/MHC class II tetramers to assess CNS-specific effector and regulatory T cells during the specific suppression of myelin proteolipid protein aa139-151 (PLP139-151)-induced experimental autoimmune encephalomyelitis (EAE) by intravenous injection of recombinant invariant chains (Ii) in which the CLIP region has been replaced by the PLP139-151 epitope (Ii-PLP139-151). Injection of Ii-PLP139-151 induced apoptosis in CNS-specific effector T cells. In contrast, the proportion of specific regulatory T cells was increased and these cells expressed larger amounts of molecules that mediate regulatory T cell function including transforming growth factor beta and the inducible costimulator (ICOS). Consequently, regulatory T cells from Ii-treated mice were more potent than regulatory T cells from control-treated animals in suppressing effector T cell proliferation. These data demonstrate that effector T cells and regulatory T cells directed against the same CNS-antigen can be differentially regulated in vivo to suppress CNS-autoimmunity. Recombinant Ii induce apoptosis in CNS-specific effector T cells and provoke qualitative changes in specific regulatory T cells that enhance their immunosuppressive properties. | lld:pubmed |
pubmed-article:19362139 | pubmed:language | eng | lld:pubmed |
pubmed-article:19362139 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19362139 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:19362139 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19362139 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19362139 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:19362139 | pubmed:month | Aug | lld:pubmed |
pubmed-article:19362139 | pubmed:issn | 1090-2139 | lld:pubmed |
pubmed-article:19362139 | pubmed:author | pubmed-author:KalbacherHube... | lld:pubmed |
pubmed-article:19362139 | pubmed:author | pubmed-author:LangeChristia... | lld:pubmed |
pubmed-article:19362139 | pubmed:author | pubmed-author:MelmsArthurA | lld:pubmed |
pubmed-article:19362139 | pubmed:author | pubmed-author:SteinbachKari... | lld:pubmed |
pubmed-article:19362139 | pubmed:author | pubmed-author:SchollMatthia... | lld:pubmed |
pubmed-article:19362139 | pubmed:author | pubmed-author:BischofFelixF | lld:pubmed |
pubmed-article:19362139 | pubmed:author | pubmed-author:DosterHongH | lld:pubmed |
pubmed-article:19362139 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:19362139 | pubmed:volume | 23 | lld:pubmed |
pubmed-article:19362139 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:19362139 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:19362139 | pubmed:pagination | 861-7 | lld:pubmed |
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pubmed-article:19362139 | pubmed:year | 2009 | lld:pubmed |
pubmed-article:19362139 | pubmed:articleTitle | Differential modulation of CNS-specific effector and regulatory T cells during tolerance induction by recombinant invariant chains in vivo. | lld:pubmed |
pubmed-article:19362139 | pubmed:affiliation | Hertie Institute for Clinical Brain Research, Department of General Neurology, University of Tübingen, Hoppe-Seyler-Strasse 3, Tübingen, Germany. | lld:pubmed |
pubmed-article:19362139 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:19362139 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |