| pubmed-article:16982873 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16982873 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:16982873 | lifeskim:mentions | umls-concept:C0004368 | lld:lifeskim |
| pubmed-article:16982873 | lifeskim:mentions | umls-concept:C1332714 | lld:lifeskim |
| pubmed-article:16982873 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:16982873 | lifeskim:mentions | umls-concept:C1515655 | lld:lifeskim |
| pubmed-article:16982873 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:16982873 | pubmed:dateCreated | 2006-9-19 | lld:pubmed |
| pubmed-article:16982873 | pubmed:abstractText | The prerequisites of peripheral activation of self-specific CD4(+) T cells that determine the development of autoimmunity are incompletely understood. SJL mice immunized with myelin proteolipid protein (PLP) 139-151 developed experimental autoimmune encephalomyelitis (EAE) when pertussis toxin (PT) was injected at the time of immunization but not when injected 6 days later, indicating that PT-induced alterations of the peripheral immune response lead to the development of autoimmunity. Further analysis using IA(s)/PLP(139-151) tetramers revealed that PT did not change effector T cell activation or regulatory T cell numbers but enhanced IFN-gamma production by self-specific CD4(+) T cells. In addition, PT promoted the generation of CD4(+)CD62L(low) effector T cells in vivo. Upon adoptive transfer, these cells were more potent than CD4(+)CD62L(high) cells in inducing autoimmunity in recipient mice. The generation of this population was paralleled by higher expression of the costimulatory molecules CD80, CD86, and B7-DC, but not B7-RP, PD-1, and B7-H1 on CD11c(+)CD4(+) dendritic cells whereas CD11c(+)CD8alpha(+) dendritic cells were not altered. Collectively, these data demonstrate the induction of autoimmunity by specific in vivo expansion of CD4(+)CD62L(low) cells and indicate that CD4(+)CD62L(low) effector T cells and CD11c(+)CD4(+) dendritic cells may be attractive targets for immune interventions to treat autoimmune diseases. | lld:pubmed |
| pubmed-article:16982873 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16982873 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16982873 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:16982873 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:16982873 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16982873 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16982873 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:16982873 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16982873 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16982873 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:16982873 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:16982873 | pubmed:author | pubmed-author:KalbacherHube... | lld:pubmed |
| pubmed-article:16982873 | pubmed:author | pubmed-author:LangeChristia... | lld:pubmed |
| pubmed-article:16982873 | pubmed:author | pubmed-author:MelmsArthurA | lld:pubmed |
| pubmed-article:16982873 | pubmed:author | pubmed-author:BischofFelixF | lld:pubmed |
| pubmed-article:16982873 | pubmed:author | pubmed-author:AmendBastianB | lld:pubmed |
| pubmed-article:16982873 | pubmed:author | pubmed-author:DosterHongH | lld:pubmed |
| pubmed-article:16982873 | pubmed:author | pubmed-author:DuboisEvelynE | lld:pubmed |
| pubmed-article:16982873 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16982873 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:16982873 | pubmed:volume | 177 | lld:pubmed |
| pubmed-article:16982873 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16982873 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16982873 | pubmed:pagination | 4384-90 | lld:pubmed |
| pubmed-article:16982873 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:16982873 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16982873 | pubmed:articleTitle | Induction of autoimmunity by expansion of autoreactive CD4+CD62Llow cells in vivo. | lld:pubmed |
| pubmed-article:16982873 | pubmed:affiliation | Hertie Institute for Clinical Brain Research, Department of General Neurology, University of Tübingen, Hoppe-Seyler-Strasse 3, 72076 Tübingen, Germany. | lld:pubmed |
| pubmed-article:16982873 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16982873 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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