|
rdf:type |
|
|
lifeskim:mentions |
|
|
pubmed:issue |
7
|
|
pubmed:dateCreated |
2004-9-20
|
|
pubmed:abstractText |
We have investigated the potential role of CD1d-restricted natural killer T (NKT) cells in the development of atherosclerosis in mice. When fed an atherogenic diet (AD), NKT cell-deficient CD1d(-/-) mice had significantly smaller atherosclerotic lesions than AD-fed C57BL/6 (wild-type [WT]) mice. A significant reduction in atherosclerotic lesions was also demonstrated in AD-fed, low-density lipoprotein receptor-deficient (Ldlr(-/-)) mice reconstituted with CD1d(-/-) bone marrow cells compared with the lesions observed in Ldlr(-/-)mice reconstituted with WT marrow cells. In addition, repeated injections of alpha-GalCer or the related glycolipid OCH to apolipoprotein E knockout (apoE(-/-)) mice during the early phase of atherosclerosis significantly enlarged the lesion areas compared with mice injected with vehicle control. However, administering alpha-GalCer to apoE(-/-) mice with established lesions did not significantly increase the lesion area but considerably decreased the collagen content. Atherosclerosis development in either AD-fed WT or apoE(-/-) mice was associated with the presence of Valpha14Jalpha18 transcripts in the atherosclerotic arterial walls, indicating that NKT cells were recruited to these lesions. Thioglycolate-elicited macrophages pulsed with oxidized low-density lipoproteins expressed enhanced CD1d levels and induced NKT cells to produce interferon-gamma, a potentially proatherogenic T-helper 1 (TH1) cytokine. Collectively, we conclude that NKT cells are proatherogenic in mice.
|
|
pubmed:grant |
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
AIM
|
|
pubmed:chemical |
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
Oct
|
|
pubmed:issn |
0006-4971
|
|
pubmed:author |
pubmed-author:BezbradicaJelena SJS,
pubmed-author:DashtsoodolNyambayarN,
pubmed-author:FujiiSatoshiS,
pubmed-author:IshimoriNaokiN,
pubmed-author:IwabuchiChikakoC,
pubmed-author:IwabuchiKazuyaK,
pubmed-author:JoyceSebastianS,
pubmed-author:KitabatakeAkiraA,
pubmed-author:MishimaTetsuyaT,
pubmed-author:MiyakeSachikoS,
pubmed-author:NakaiYukihitoY,
pubmed-author:NakayamaToshinoriT,
pubmed-author:OnoéKazunoriK,
pubmed-author:TanakaShinyaS,
pubmed-author:TaniguchiMasaruM,
pubmed-author:Van KaerLucL,
pubmed-author:WatanoKeikoK,
pubmed-author:YamamuraTakashiT
|
|
pubmed:issnType |
Print
|
|
pubmed:day |
1
|
|
pubmed:volume |
104
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
2051-9
|
|
pubmed:dateRevised |
2008-11-21
|
|
pubmed:meshHeading |
pubmed-meshheading:15113755-Animals,
pubmed-meshheading:15113755-Antigens, CD1,
pubmed-meshheading:15113755-Antigens, CD1d,
pubmed-meshheading:15113755-Apolipoproteins E,
pubmed-meshheading:15113755-Arteriosclerosis,
pubmed-meshheading:15113755-Bone Marrow Cells,
pubmed-meshheading:15113755-Bone Marrow Transplantation,
pubmed-meshheading:15113755-Diet, Atherogenic,
pubmed-meshheading:15113755-Flow Cytometry,
pubmed-meshheading:15113755-Glycolipids,
pubmed-meshheading:15113755-Interferon-gamma,
pubmed-meshheading:15113755-Killer Cells, Natural,
pubmed-meshheading:15113755-Leukocytes, Mononuclear,
pubmed-meshheading:15113755-Mice,
pubmed-meshheading:15113755-Mice, Inbred C57BL,
pubmed-meshheading:15113755-Mice, Knockout,
pubmed-meshheading:15113755-Mice, Transgenic,
pubmed-meshheading:15113755-RNA, Messenger,
pubmed-meshheading:15113755-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:15113755-Spleen,
pubmed-meshheading:15113755-T-Lymphocytes,
pubmed-meshheading:15113755-Th1 Cells,
pubmed-meshheading:15113755-Time Factors,
pubmed-meshheading:15113755-Transgenes
|
|
pubmed:year |
2004
|
|
pubmed:articleTitle |
Natural killer T cells accelerate atherogenesis in mice.
|
|
pubmed:affiliation |
Division of Immunobiology, Research Section of Pathophysiology, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan.
|
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|
