pubmed-article:15254597 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:15254597 | lifeskim:mentions | umls-concept:C0021368 | lld:lifeskim |
pubmed-article:15254597 | lifeskim:mentions | umls-concept:C0002940 | lld:lifeskim |
pubmed-article:15254597 | lifeskim:mentions | umls-concept:C0003483 | lld:lifeskim |
pubmed-article:15254597 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
pubmed-article:15254597 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
pubmed-article:15254597 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
pubmed-article:15254597 | lifeskim:mentions | umls-concept:C0332206 | lld:lifeskim |
pubmed-article:15254597 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:15254597 | pubmed:dateCreated | 2004-7-15 | lld:pubmed |
pubmed-article:15254597 | pubmed:abstractText | Abdominal aortic aneurysms (AAAs) cause death due to complications related to expansion and rupture. The underlying mechanisms that drive AAA development remain largely unknown. We recently described evidence for a shift toward T helper type 2 (Th2) cell responses in human AAAs compared with stenotic atheromas. To evaluate putative pathways in AAA formation, we induced Th1- or Th2-predominant cytokine environments in an inflammatory aortic lesion using murine aortic transplantation into WT hosts or those lacking the receptors for the hallmark Th1 cytokine IFN-gamma, respectively. Allografts in WT recipients developed intimal hyperplasia, whereas allografts in IFN-gamma receptor-deficient (GRKO) hosts developed severe AAA formation associated with markedly increased levels of MMP-9 and MMP-12. Allografts in GRKO recipients treated with anti-IL-4 antibody to block the characteristic IL-4 Th2 cytokine or allografts in GRKO hosts also congenitally deficient in IL-4 did not develop AAA and likewise exhibited attenuated collagenolytic and elastolytic activities. These observations demonstrate an important dichotomy between cellular immune responses that induce IFN-gamma- or IL-4-dominated cytokine environments. The findings establish important regulatory roles for a Th1/Th2 cytokine balance in modulating matrix remodeling and have important implications for the pathophysiology of AAAs and arteriosclerosis. | lld:pubmed |
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pubmed-article:15254597 | pubmed:language | eng | lld:pubmed |
pubmed-article:15254597 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15254597 | pubmed:citationSubset | AIM | lld:pubmed |
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pubmed-article:15254597 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:15254597 | pubmed:month | Jul | lld:pubmed |
pubmed-article:15254597 | pubmed:issn | 0021-9738 | lld:pubmed |
pubmed-article:15254597 | pubmed:author | pubmed-author:ShichiriMasay... | lld:pubmed |
pubmed-article:15254597 | pubmed:author | pubmed-author:LibbyPeterP | lld:pubmed |
pubmed-article:15254597 | pubmed:author | pubmed-author:LeeRichard... | lld:pubmed |
pubmed-article:15254597 | pubmed:author | pubmed-author:MitchellRicha... | lld:pubmed |
pubmed-article:15254597 | pubmed:author | pubmed-author:ShimizuKoichi... | lld:pubmed |
pubmed-article:15254597 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:15254597 | pubmed:volume | 114 | lld:pubmed |
pubmed-article:15254597 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:15254597 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:15254597 | pubmed:pagination | 300-8 | lld:pubmed |
pubmed-article:15254597 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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