| pubmed-article:12566416 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12566416 | lifeskim:mentions | umls-concept:C0027059 | lld:lifeskim |
| pubmed-article:12566416 | lifeskim:mentions | umls-concept:C0011306 | lld:lifeskim |
| pubmed-article:12566416 | lifeskim:mentions | umls-concept:C0063710 | lld:lifeskim |
| pubmed-article:12566416 | lifeskim:mentions | umls-concept:C0443146 | lld:lifeskim |
| pubmed-article:12566416 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:12566416 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:12566416 | lifeskim:mentions | umls-concept:C1511545 | lld:lifeskim |
| pubmed-article:12566416 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:12566416 | pubmed:dateCreated | 2003-2-4 | lld:pubmed |
| pubmed-article:12566416 | pubmed:abstractText | Dilated cardiomyopathy, resulting from myocarditis, is the most common cause of heart failure in young patients. We here show that interleukin (IL)-1 receptor type 1-deficient (IL-1R1(-/-)) mice are protected from development of autoimmune myocarditis after immunization with alpha-myosin-peptide(614-629). CD4(+) T cells from immunized IL-1R1(-/-) mice proliferated poorly and failed to transfer disease after injection into naive severe combined immunodeficiency (SCID) mice. In vitro stimulation experiments suggested that the function of IL-1R1(-/-)CD4(+) T cells was not intrinsically defect, but their activation by dendritic cells was impaired in IL-1R1(-/-) mice. Accordingly, production of tumor necrosis factor (TNF)-alpha, IL-1, IL-6, and IL-12p70 was reduced in dendritic cells lacking the IL-1 receptor type 1. In fact, injection of immature, antigen-loaded IL-1R1(+/+) but not IL-1R1(-/-) dendritic cells into IL-1R1(-/-) mice fully restored disease susceptibility by rendering IL-1R1(-/-) CD4(+) T cells pathogenic. Thus, IL-1R1 triggering is required for efficient activation of dendritic cells, which is in turn a prerequisite for induction of autoreactive CD4(+) T cells and autoimmunity. | lld:pubmed |
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| pubmed-article:12566416 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12566416 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12566416 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12566416 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12566416 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:12566416 | pubmed:issn | 0022-1007 | lld:pubmed |
| pubmed-article:12566416 | pubmed:author | pubmed-author:PenningerJose... | lld:pubmed |
| pubmed-article:12566416 | pubmed:author | pubmed-author:KopfManfredM | lld:pubmed |
| pubmed-article:12566416 | pubmed:author | pubmed-author:HunzikerLukas... | lld:pubmed |
| pubmed-article:12566416 | pubmed:author | pubmed-author:ErikssonUrsU | lld:pubmed |
| pubmed-article:12566416 | pubmed:author | pubmed-author:SuzukiShinobu... | lld:pubmed |
| pubmed-article:12566416 | pubmed:author | pubmed-author:KurrerMichael... | lld:pubmed |
| pubmed-article:12566416 | pubmed:author | pubmed-author:TafuriAnnaA | lld:pubmed |
| pubmed-article:12566416 | pubmed:author | pubmed-author:SondereggerIv... | lld:pubmed |
| pubmed-article:12566416 | pubmed:author | pubmed-author:IezziGiandome... | lld:pubmed |
| pubmed-article:12566416 | pubmed:author | pubmed-author:BachmaierKurt... | lld:pubmed |
| pubmed-article:12566416 | pubmed:author | pubmed-author:BingisserRola... | lld:pubmed |
| pubmed-article:12566416 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12566416 | pubmed:day | 3 | lld:pubmed |
| pubmed-article:12566416 | pubmed:volume | 197 | lld:pubmed |
| pubmed-article:12566416 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12566416 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12566416 | pubmed:pagination | 323-31 | lld:pubmed |
| pubmed-article:12566416 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:12566416 | pubmed:meshHeading | pubmed-meshheading:12566416... | lld:pubmed |
| pubmed-article:12566416 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:12566416 | pubmed:articleTitle | Activation of dendritic cells through the interleukin 1 receptor 1 is critical for the induction of autoimmune myocarditis. | lld:pubmed |
