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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.

Original publication




Journal article



Publication Date





2051 - 2059


Animals, Antigens, CD1, Antigens, CD1d, Apolipoproteins E, Arteriosclerosis, Bone Marrow Cells, Bone Marrow Transplantation, Diet, Atherogenic, Flow Cytometry, Glycolipids, Interferon-gamma, Killer Cells, Natural, Leukocytes, Mononuclear, Mice, Mice, Inbred C57BL, Mice, Knockout, Mice, Transgenic, RNA, Messenger, Reverse Transcriptase Polymerase Chain Reaction, Spleen, T-Lymphocytes, Th1 Cells, Time Factors, Transgenes