| pubmed-article:20378858 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20378858 | lifeskim:mentions | umls-concept:C0027059 | lld:lifeskim |
| pubmed-article:20378858 | lifeskim:mentions | umls-concept:C0007193 | lld:lifeskim |
| pubmed-article:20378858 | lifeskim:mentions | umls-concept:C0449258 | lld:lifeskim |
| pubmed-article:20378858 | lifeskim:mentions | umls-concept:C1705947 | lld:lifeskim |
| pubmed-article:20378858 | lifeskim:mentions | umls-concept:C0205224 | lld:lifeskim |
| pubmed-article:20378858 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:20378858 | pubmed:dateCreated | 2010-5-28 | lld:pubmed |
| pubmed-article:20378858 | pubmed:abstractText | One-third of myocarditis cases progresses to dilated cardiomyopathy (DCM), but the mechanisms controlling this process are largely unknown. CD4(+) T helper (Th)17 cells have been implicated in the pathogenesis of autoimmune diseases, but the role of Th17-produced cytokines during inflammation-induced cardiac remodeling has not been previously studied. | lld:pubmed |
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| pubmed-article:20378858 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20378858 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20378858 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:20378858 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20378858 | pubmed:month | May | lld:pubmed |
| pubmed-article:20378858 | pubmed:issn | 1524-4571 | lld:pubmed |
| pubmed-article:20378858 | pubmed:author | pubmed-author:IwakuraYoichi... | lld:pubmed |
| pubmed-article:20378858 | pubmed:author | pubmed-author:RoseNoel RNR | lld:pubmed |
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| pubmed-article:20378858 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20378858 | pubmed:day | 28 | lld:pubmed |
| pubmed-article:20378858 | pubmed:volume | 106 | lld:pubmed |
| pubmed-article:20378858 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20378858 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20378858 | pubmed:pagination | 1646-55 | lld:pubmed |
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| pubmed-article:20378858 | pubmed:year | 2010 | lld:pubmed |
| pubmed-article:20378858 | pubmed:articleTitle | Interleukin-17A is dispensable for myocarditis but essential for the progression to dilated cardiomyopathy. | lld:pubmed |
| pubmed-article:20378858 | pubmed:affiliation | Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. | lld:pubmed |
| pubmed-article:20378858 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:20378858 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:20378858 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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